Hemodynamic effects of clonidine in two contrasting models of autonomic failure: Multiple system atrophy and pure autonomic failure
We assessed the effects of clonidine on blood pressure (BP) and heart rate (HR) in multiple system atrophy (MSA), where the autonomic nervous system lesion site is preganglionic, and in pure autonomic failure (PAF), where it is postganglionic. In normal subjects, intravenous infusion of the selectiv...
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| Published in | Movement Disorders Vol. 21; no. 5; pp. 609 - 615 |
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| Main Authors | , , , |
| Format | Journal Article |
| Language | English |
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01.05.2006
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| ISSN | 0885-3185 1531-8257 |
| DOI | 10.1002/mds.20755 |
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| Abstract | We assessed the effects of clonidine on blood pressure (BP) and heart rate (HR) in multiple system atrophy (MSA), where the autonomic nervous system lesion site is preganglionic, and in pure autonomic failure (PAF), where it is postganglionic. In normal subjects, intravenous infusion of the selective α2‐adrenoceptor agonist clonidine reduces BP and plasma noradrenaline (NA) levels by means of central α2‐adrenoceptor action, as well as inducing growth hormone (GH) release. Clonidine‐induced GH release is impaired in MSA but spared in PAF. However, the hemodynamic effects of clonidine have not been studied extensively in these disorders. We examined intravenous clonidine test results (performed in our autonomic laboratories using the London Autonomic Units protocol) in 58 patients: 39 with probable MSA and 19 with PAF. Systolic BP (SBP), diastolic BP (DBP), HR, and NA levels were measured supine at baseline and for up to 60 minutes after clonidine. Clonidine resulted in a significant BP fall in MSA patients, which occurred earlier (within 15 minutes of clonidine) and to a greater extent than seen in PAF patients. MSA and PAF patients showed reduction in HR after clonidine administration, although this finding was significantly greater in MSA than in PAF patients. NA levels decreased significantly after clonidine administration in both groups. Although basal NA levels were lower in PAF than in MSA patients, there was no difference in NA reduction relative to baseline between groups. MSA patients showed significant negative correlation between basal NA levels and BP response to clonidine. Clonidine infusion reduces BP and HR in both MSA and PAF groups but to a greater extent in MSA patients. The greater vasodepressor action of clonidine in MSA patients suggests that there is partial preservation of brainstem sympathetic outflow pathways in MSA and may reflect its action at sites in the brainstem and spinal cord that were in part functionally preserved in MSA. Despite similar degrees of NA reduction after clonidine administration, the vasodepressor effect of clonidine was attenuated in PAF compared with MSA patients. This attenuation in PAF patients may reflect greater peripheral α2‐adrenoceptor denervation supersensitivity due to the postganglionic lesion site. These BP differences, thus, may reflect the underlying lesion site in MSA and PAF, and the hemodynamic data after clonidine infusion may help differentiate these conditions. © 2006 Movement Disorder Society |
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| AbstractList | We assessed the effects of clonidine on blood pressure (BP) and heart rate (HR) in multiple system atrophy (MSA), where the autonomic nervous system lesion site is preganglionic, and in pure autonomic failure (PAF), where it is postganglionic. In normal subjects, intravenous infusion of the selective alpha2-adrenoceptor agonist clonidine reduces BP and plasma noradrenaline (NA) levels by means of central alpha2-adrenoceptor action, as well as inducing growth hormone (GH) release. Clonidine-induced GH release is impaired in MSA but spared in PAF. However, the hemodynamic effects of clonidine have not been studied extensively in these disorders. We examined intravenous clonidine test results (performed in our autonomic laboratories using the London Autonomic Units protocol) in 58 patients: 39 with probable MSA and 19 with PAF. Systolic BP (SBP), diastolic BP (DBP), HR, and NA levels were measured supine at baseline and for up to 60 minutes after clonidine. Clonidine resulted in a significant BP fall in MSA patients, which occurred earlier (within 15 minutes of clonidine) and to a greater extent than seen in PAF patients. MSA and PAF patients showed reduction in HR after clonidine administration, although this finding was significantly greater in MSA than in PAF patients. NA levels decreased significantly after clonidine administration in both groups. Although basal NA levels were lower in PAF than in MSA patients, there was no difference in NA reduction relative to baseline between groups. MSA patients showed significant negative correlation between basal NA levels and BP response to clonidine. Clonidine infusion reduces BP and HR in both MSA and PAF groups but to a greater extent in MSA patients. The greater vasodepressor action of clonidine in MSA patients suggests that there is partial preservation of brainstem sympathetic outflow pathways in MSA and may reflect its action at sites in the brainstem and spinal cord that were in part functionally preserved in MSA. Despite similar degrees of NA reduction after clonidine administration, the vasodepressor effect of clonidine was attenuated in PAF compared with MSA patients. This attenuation in PAF patients may reflect greater peripheral alpha2-adrenoceptor denervation supersensitivity due to the postganglionic lesion site. These BP differences, thus, may reflect the underlying lesion site in MSA and PAF, and the hemodynamic data after clonidine infusion may help differentiate these conditions.We assessed the effects of clonidine on blood pressure (BP) and heart rate (HR) in multiple system atrophy (MSA), where the autonomic nervous system lesion site is preganglionic, and in pure autonomic failure (PAF), where it is postganglionic. In normal subjects, intravenous infusion of the selective alpha2-adrenoceptor agonist clonidine reduces BP and plasma noradrenaline (NA) levels by means of central alpha2-adrenoceptor action, as well as inducing growth hormone (GH) release. Clonidine-induced GH release is impaired in MSA but spared in PAF. However, the hemodynamic effects of clonidine have not been studied extensively in these disorders. We examined intravenous clonidine test results (performed in our autonomic laboratories using the London Autonomic Units protocol) in 58 patients: 39 with probable MSA and 19 with PAF. Systolic BP (SBP), diastolic BP (DBP), HR, and NA levels were measured supine at baseline and for up to 60 minutes after clonidine. Clonidine resulted in a significant BP fall in MSA patients, which occurred earlier (within 15 minutes of clonidine) and to a greater extent than seen in PAF patients. MSA and PAF patients showed reduction in HR after clonidine administration, although this finding was significantly greater in MSA than in PAF patients. NA levels decreased significantly after clonidine administration in both groups. Although basal NA levels were lower in PAF than in MSA patients, there was no difference in NA reduction relative to baseline between groups. MSA patients showed significant negative correlation between basal NA levels and BP response to clonidine. Clonidine infusion reduces BP and HR in both MSA and PAF groups but to a greater extent in MSA patients. The greater vasodepressor action of clonidine in MSA patients suggests that there is partial preservation of brainstem sympathetic outflow pathways in MSA and may reflect its action at sites in the brainstem and spinal cord that were in part functionally preserved in MSA. Despite similar degrees of NA reduction after clonidine administration, the vasodepressor effect of clonidine was attenuated in PAF compared with MSA patients. This attenuation in PAF patients may reflect greater peripheral alpha2-adrenoceptor denervation supersensitivity due to the postganglionic lesion site. These BP differences, thus, may reflect the underlying lesion site in MSA and PAF, and the hemodynamic data after clonidine infusion may help differentiate these conditions. We assessed the effects of clonidine on blood pressure (BP) and heart rate (HR) in multiple system atrophy (MSA), where the autonomic nervous system lesion site is preganglionic, and in pure autonomic failure (PAF), where it is postganglionic. In normal subjects, intravenous infusion of the selective 2-adrenoceptor agonist clonidine reduces BP and plasma noradrenaline (NA) levels by means of central 2-adrenoceptor action, as well as inducing growth hormone (GH) release. Clonidine-induced GH release is impaired in MSA but spared in PAF. However, the hemodynamic effects of clonidine have not been studied extensively in these disorders. We examined intravenous clonidine test results (performed in our autonomic laboratories using the London Autonomic Units protocol) in 58 patients: 39 with probable MSA and 19 with PAF. Systolic BP (SBP), diastolic BP (DBP), HR, and NA levels were measured supine at baseline and for up to 60 minutes after clonidine. Clonidine resulted in a significant BP fall in MSA patients, which occurred earlier (within 15 minutes of clonidine) and to a greater extent than seen in PAF patients. MSA and PAF patients showed reduction in HR after clonidine administration, although this finding was significantly greater in MSA than in PAF patients. NA levels decreased significantly after clonidine administration in both groups. Although basal NA levels were lower in PAF than in MSA patients, there was no difference in NA reduction relative to baseline between groups. MSA patients showed significant negative correlation between basal NA levels and BP response to clonidine. Clonidine infusion reduces BP and HR in both MSA and PAF groups but to a greater extent in MSA patients. The greater vasodepressor action of clonidine in MSA patients suggests that there is partial preservation of brainstem sympathetic outflow pathways in MSA and may reflect its action at sites in the brainstem and spinal cord that were in part functionally preserved in MSA. Despite similar degrees of NA reduction after clonidine administration, the vasodepressor effect of clonidine was attenuated in PAF compared with MSA patients. This attenuation in PAF patients may reflect greater peripheral 2-adrenoceptor denervation supersensitivity due to the postganglionic lesion site. These BP differences, thus, may reflect the underlying lesion site in MSA and PAF, and the hemodynamic data after clonidine infusion may help differentiate these conditions. We assessed the effects of clonidine on blood pressure (BP) and heart rate (HR) in multiple system atrophy (MSA), where the autonomic nervous system lesion site is preganglionic, and in pure autonomic failure (PAF), where it is postganglionic. In normal subjects, intravenous infusion of the selective α2‐adrenoceptor agonist clonidine reduces BP and plasma noradrenaline (NA) levels by means of central α2‐adrenoceptor action, as well as inducing growth hormone (GH) release. Clonidine‐induced GH release is impaired in MSA but spared in PAF. However, the hemodynamic effects of clonidine have not been studied extensively in these disorders. We examined intravenous clonidine test results (performed in our autonomic laboratories using the London Autonomic Units protocol) in 58 patients: 39 with probable MSA and 19 with PAF. Systolic BP (SBP), diastolic BP (DBP), HR, and NA levels were measured supine at baseline and for up to 60 minutes after clonidine. Clonidine resulted in a significant BP fall in MSA patients, which occurred earlier (within 15 minutes of clonidine) and to a greater extent than seen in PAF patients. MSA and PAF patients showed reduction in HR after clonidine administration, although this finding was significantly greater in MSA than in PAF patients. NA levels decreased significantly after clonidine administration in both groups. Although basal NA levels were lower in PAF than in MSA patients, there was no difference in NA reduction relative to baseline between groups. MSA patients showed significant negative correlation between basal NA levels and BP response to clonidine. Clonidine infusion reduces BP and HR in both MSA and PAF groups but to a greater extent in MSA patients. The greater vasodepressor action of clonidine in MSA patients suggests that there is partial preservation of brainstem sympathetic outflow pathways in MSA and may reflect its action at sites in the brainstem and spinal cord that were in part functionally preserved in MSA. Despite similar degrees of NA reduction after clonidine administration, the vasodepressor effect of clonidine was attenuated in PAF compared with MSA patients. This attenuation in PAF patients may reflect greater peripheral α2‐adrenoceptor denervation supersensitivity due to the postganglionic lesion site. These BP differences, thus, may reflect the underlying lesion site in MSA and PAF, and the hemodynamic data after clonidine infusion may help differentiate these conditions. © 2006 Movement Disorder Society We assessed the effects of clonidine on blood pressure (BP) and heart rate (HR) in multiple system atrophy (MSA), where the autonomic nervous system lesion site is preganglionic, and in pure autonomic failure (PAF), where it is postganglionic. In normal subjects, intravenous infusion of the selective alpha2-adrenoceptor agonist clonidine reduces BP and plasma noradrenaline (NA) levels by means of central alpha2-adrenoceptor action, as well as inducing growth hormone (GH) release. Clonidine-induced GH release is impaired in MSA but spared in PAF. However, the hemodynamic effects of clonidine have not been studied extensively in these disorders. We examined intravenous clonidine test results (performed in our autonomic laboratories using the London Autonomic Units protocol) in 58 patients: 39 with probable MSA and 19 with PAF. Systolic BP (SBP), diastolic BP (DBP), HR, and NA levels were measured supine at baseline and for up to 60 minutes after clonidine. Clonidine resulted in a significant BP fall in MSA patients, which occurred earlier (within 15 minutes of clonidine) and to a greater extent than seen in PAF patients. MSA and PAF patients showed reduction in HR after clonidine administration, although this finding was significantly greater in MSA than in PAF patients. NA levels decreased significantly after clonidine administration in both groups. Although basal NA levels were lower in PAF than in MSA patients, there was no difference in NA reduction relative to baseline between groups. MSA patients showed significant negative correlation between basal NA levels and BP response to clonidine. Clonidine infusion reduces BP and HR in both MSA and PAF groups but to a greater extent in MSA patients. The greater vasodepressor action of clonidine in MSA patients suggests that there is partial preservation of brainstem sympathetic outflow pathways in MSA and may reflect its action at sites in the brainstem and spinal cord that were in part functionally preserved in MSA. Despite similar degrees of NA reduction after clonidine administration, the vasodepressor effect of clonidine was attenuated in PAF compared with MSA patients. This attenuation in PAF patients may reflect greater peripheral alpha2-adrenoceptor denervation supersensitivity due to the postganglionic lesion site. These BP differences, thus, may reflect the underlying lesion site in MSA and PAF, and the hemodynamic data after clonidine infusion may help differentiate these conditions. |
| Author | Young, Tim M. Asahina, Masato Watson, Laura Mathias, Christopher J. |
| Author_xml | – sequence: 1 givenname: Tim M. surname: Young fullname: Young, Tim M. email: tim.young@imperial.ac.uk organization: Neurovascular Medicine Unit, Faculty of Medicine, Imperial College London at St. Mary's Hospital, London, United Kingdom – sequence: 2 givenname: Masato surname: Asahina fullname: Asahina, Masato organization: Neurovascular Medicine Unit, Faculty of Medicine, Imperial College London at St. Mary's Hospital, London, United Kingdom – sequence: 3 givenname: Laura surname: Watson fullname: Watson, Laura organization: Neurovascular Medicine Unit, Faculty of Medicine, Imperial College London at St. Mary's Hospital, London, United Kingdom – sequence: 4 givenname: Christopher J. surname: Mathias fullname: Mathias, Christopher J. organization: Neurovascular Medicine Unit, Faculty of Medicine, Imperial College London at St. Mary's Hospital, London, United Kingdom |
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| Cites_doi | 10.1097/00004872-199715011-00007 10.1054/ghir.2001.0199 10.1172/JCI112611 10.1161/01.HYP.34.4.1012 10.1016/S0140-6736(96)10168-9 10.1002/cpt1977215593 10.1016/0014-2999(89)90597-9 10.1097/00005344-199424001-00002 10.1016/0165-0173(84)90030-4 10.1046/j.1365-2044.1999.00659.x 10.1007/BF01818957 10.1042/cs057425s 10.1016/0006-8993(87)90941-3 10.1016/j.autneu.2003.08.011 10.1161/01.CIR.84.1.75 10.1016/S0009-9236(03)00087-0 10.1016/0140-6736(92)92355-J 10.1212/WNL.43.6.1181 10.1016/S0378-4347(00)80506-X 10.1042/cs0750071 10.1038/clpt.1989.113 10.1159/000138321 10.1002/cpt1977214375 10.1038/clpt.1983.216 10.1016/0014-2999(73)90122-2 10.1161/01.HYP.30.1.83 10.1007/BF00314991 |
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| Keywords | pure autonomic failure Nervous system diseases Diseases of the autonomic nervous system Multiple system atrophy Arterial pressure Clonidine Models Blood pressure Hemodynamics |
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| References | Nurnberger J, Dammer S, Mitchell A, et al. Effect of the C825T polymorphism of the G protein beta3 subunit on the systolic blood pressure-lowering effect of clonidine in young, healthy male subjects. Clin Pharmacol Ther 2003; 74: 53-60. Tsai ML, Lin MT. Participation of a bulbospinal serotonergic pathway in the rat brain in clonidine-induced hypotension and bradycardia. Pharmacology 1987; 35: 279-285. Kiowski W, Hulthen UL, Ritz R, Buhler FR. Alpha-2 adrenoceptor-mediated vasoconstriction of arteries. Clin Pharmacol Ther 1983; 34: 365-369. Kimber JR, Watson L, Mathias CJ. Distinction of idiopathic Parkinson's disease from multiple system atrophy by stimulation of growth hormone release with clonidine. Lancet 1997; 349: 1877-1881. Davies DS, Wing AM, Reid JL, Neill DM, Tippet P, Dollery CT. Pharmacokinetics and concentration-effects of intravenous and oral clonidine. Clin Pharmacol Ther 1977; 21: 593-601. Mathias CJ, Reid JL, Wing LM, Frankel HL, Christensen NJ. Antihypertensive effects of clonidine in tetraplegic subjects devoid of central sympathetic control. Clin Sci 1979; 57(Suppl. 5): 425s-428s. Sinha JN, Atkinson JM, Schmitt H. Effects of clonidine and L-dopa on spontaneous and evoked splanchnic nerve discharges. Eur J Pharmacol 1973; 24: 113-119. Bricca G, Dontenwill M, Molines A, Feldman J, Belcourt A, Bousquet P. The imidazoline preferring receptor: binding studies in bovine, rat and human brain stem. Eur J Pharmacol 1989; 162: 1-9. Zoukos Y, Thomaides T, Pavitt DV, Cuzner ML, Mathias CJ. Beta-adrenoceptor expression on circulating mononuclear cells of idiopathic Parkinson's disease and autonomic failure patients before and after reduction of central sympathetic outflow by clonidine. Neurology 1993; 43: 1181-1187. Thomaides TN, Chaudhuri KR, Maule S, Watson L, Marsden CD, Mathias CJ. Growth hormone response to clonidine in central and peripheral primary autonomic failure. Lancet 1992; 340: 263-266. Khan ZP, Ferguson CN, Jones RM. Alpha-2 and imidazoline receptor agonists. Anaesthesia 1999; 54: 146-165. Petty M, Reid JL, Tangri KK. The cardiovascular effects of clonidine in rabbits after cervical spinal cord transection. Br J Pharmacol 1976; 57: 449P-450P. Unnerstall JR, Kopajtic TA, Kuhar MJ. Distribution of alpha 2 agonist binding sites in the rat and human central nervous system: analysis of some functional, anatomic correlates of the pharmacologic effects of clonidine and related adrenergic agents. Brain Res 1984; 319: 69-101. Onrot J, Goldberg MR, Biaggioni I, Hollister AS, Kincaid D, Robertson D. Postjunctional vascular smooth muscle alpha-2 adrenoreceptors in human autonomic failure. Clin Invest Med 1987; 10: 26-31. Kroin JS, McCarthy RJ, Penn RD, Lubenow TR, Ivankovich AD. Intrathecal clonidine and tizanidine in conscious dogs: comparison of analgesic and hemodynamic effects. Anesth Analg 1996; 82: 627-635. Haxhiu MA, Dreshaj I, Schäfer SG, Ernsberger P. Selective antihypertensive action of moxonidine is mediated mainly by I1-imidazoline receptors in the rostral ventrolateral medulla. J Cardiovasc Pharmacol 1994; 24(Suppl. 1): S1-S8. Kooner JS, Birch R, Frankel HL, Peart WS, Mathias CJ. Haemodynamic and neurohormonal effects of clonidine in patients with preganglionic and postganglionic sympathetic lesions. Evidence for a central sympatholytic action. Circulation 1991; 34: 75-83. Mathias CJ, Bannister R, Cortelli P, et al. Clinical autonomic and therapeutic observations in two siblings with postural hypotension and sympathetic failure due to an inability to synthesize noradrenaline from dopamine because of a deficiency of dopamine beta hydroxylase. Q J Med 1990; 278: 617-633. da Costa DF, Bannister R, Landon J, Mathias CJ. Growth hormone response to clonidine is impaired in patients with central sympathetic degeneration. Clin Exp Hypertens A 1984; 6: 1843-1846. Smedes F, Kraak JC, Poppe H. A simple and fast solvent extraction system for selective and quantitative isolation of adrenaline, noradrenaline and dopamine from plasma and urine. J Chromatogr 1982; 231: 25-39. Reid JL, Wing LM, Mathias CJ, Frankel HL, Neill E. The central hypotensive effect of clonidine. Studies in tetraplegic subjects. Clin Pharmacol Ther 1977; 21: 375-381. Wang WZ, Yuan WJ, Su DF. Blockade of N-methyl-D-aspartate receptors within the rostral ventrolateral medulla antagonizes clonidine-induced cardiovascular effects. Auton Neurosci 2003; 109: 21-28. Isaac L. Brain sites for the antihypertensive effects of clonidine. Prog Clin Biol Res 1981; 71: 29-39. Warren JB, Dollery CT, Fuller RW, Williams MS, Gertz BJ. Assessment of MK-912, an α2-adrenoceptor antagonist, with use of intravenous clonidine. Clin Pharmacol Ther 1989; 46: 103-109. Kimber J, Sivenandan M, Watson L, Mathias CJ. Age- and gender-related growth hormone responses to intravenous clonidine in healthy adults Growth Horm IGF Res 2001; 11: 128-135. May CN, Ham IW, Heslop KE, Stone FA, Mathias CJ. Intravenous morphine causes hypertension, hyperglycaemia and increases sympatho-adrenal outflow in conscious rabbits. Clin Sci 1988; 75: 71-77. Prichard BN, Graham BR. The use of moxonidine in the treatment of hypertension. J Hypertens Suppl 1997; 15: S47-S55. Senard JM, Arias A, Berlan M, Tran MA, Rascol A, Montastruc JL. Pharmacological evidence of alpha 1- and alpha 2-adrenergic supersensitivity in orthostatic hypotension due to spinal cord injury: a case report. Eur J Clin Pharmacol 1991; 41: 593-596. Zoukos Y, Thomaides T, Pavitt DV, Leonard JP, Cuzner ML, Mathias CJ. Up-regulation of beta-adrenoceptors on circulating mononuclear cells after reduction of central sympathetic outflow by clonidine in normal subjects. Clin Auton Res 1992; 2: 165-170. Punnen S. Urbanski R, Krieger AJ, Sapru HN. Ventrolateral medullary pressor area: site of hypotensive action of clonidine. Brain Res 1987 422: 336-346. Pompermayer K, Salgado MC, Feldman J, Bousquet P. Cardiovascular effects of clonidine-like drugs in pithed rabbits. Hypertension 1999; 34: 1012-1015. Robertson D, Goldberg MR, Tung CS, Hollister AS, Robertson RM. Use of alpha 2 adrenoreceptor agonists and antagonists in the functional assessment of the sympathetic nervous system. J Clin Invest 1986; 78: 576-581. Gilman S, Low PA, Quinn N, et al. Consensus statement on the diagnosis of multiple system atrophy. J Auton Nerv Syst 1998; 74: 189-192. Mukaddam-Daher S, Lambert C, Gutkowska J. Clonidine and ST-91 may activate imidazoline binding sites in the heart to release atrial natriuretic peptide. 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| References_xml | – reference: Kimber J, Sivenandan M, Watson L, Mathias CJ. Age- and gender-related growth hormone responses to intravenous clonidine in healthy adults Growth Horm IGF Res 2001; 11: 128-135. – reference: Wang WZ, Yuan WJ, Su DF. Blockade of N-methyl-D-aspartate receptors within the rostral ventrolateral medulla antagonizes clonidine-induced cardiovascular effects. Auton Neurosci 2003; 109: 21-28. – reference: Pompermayer K, Salgado MC, Feldman J, Bousquet P. Cardiovascular effects of clonidine-like drugs in pithed rabbits. Hypertension 1999; 34: 1012-1015. – reference: May CN, Ham IW, Heslop KE, Stone FA, Mathias CJ. Intravenous morphine causes hypertension, hyperglycaemia and increases sympatho-adrenal outflow in conscious rabbits. Clin Sci 1988; 75: 71-77. – reference: Warren JB, Dollery CT, Fuller RW, Williams MS, Gertz BJ. Assessment of MK-912, an α2-adrenoceptor antagonist, with use of intravenous clonidine. Clin Pharmacol Ther 1989; 46: 103-109. – reference: Zoukos Y, Thomaides T, Pavitt DV, Leonard JP, Cuzner ML, Mathias CJ. Up-regulation of beta-adrenoceptors on circulating mononuclear cells after reduction of central sympathetic outflow by clonidine in normal subjects. Clin Auton Res 1992; 2: 165-170. – reference: Punnen S. Urbanski R, Krieger AJ, Sapru HN. Ventrolateral medullary pressor area: site of hypotensive action of clonidine. Brain Res 1987 422: 336-346. – reference: Mathias CJ, Bannister R, Cortelli P, et al. Clinical autonomic and therapeutic observations in two siblings with postural hypotension and sympathetic failure due to an inability to synthesize noradrenaline from dopamine because of a deficiency of dopamine beta hydroxylase. Q J Med 1990; 278: 617-633. – reference: Kooner JS, Birch R, Frankel HL, Peart WS, Mathias CJ. Haemodynamic and neurohormonal effects of clonidine in patients with preganglionic and postganglionic sympathetic lesions. Evidence for a central sympatholytic action. Circulation 1991; 34: 75-83. – reference: Petty M, Reid JL, Tangri KK. The cardiovascular effects of clonidine in rabbits after cervical spinal cord transection. Br J Pharmacol 1976; 57: 449P-450P. – reference: Unnerstall JR, Kopajtic TA, Kuhar MJ. Distribution of alpha 2 agonist binding sites in the rat and human central nervous system: analysis of some functional, anatomic correlates of the pharmacologic effects of clonidine and related adrenergic agents. Brain Res 1984; 319: 69-101. – reference: Gilman S, Low PA, Quinn N, et al. Consensus statement on the diagnosis of multiple system atrophy. J Auton Nerv Syst 1998; 74: 189-192. – reference: Kroin JS, McCarthy RJ, Penn RD, Lubenow TR, Ivankovich AD. Intrathecal clonidine and tizanidine in conscious dogs: comparison of analgesic and hemodynamic effects. Anesth Analg 1996; 82: 627-635. – reference: Mathias CJ, Reid JL, Wing LM, Frankel HL, Christensen NJ. Antihypertensive effects of clonidine in tetraplegic subjects devoid of central sympathetic control. Clin Sci 1979; 57(Suppl. 5): 425s-428s. – reference: Davies DS, Wing AM, Reid JL, Neill DM, Tippet P, Dollery CT. Pharmacokinetics and concentration-effects of intravenous and oral clonidine. Clin Pharmacol Ther 1977; 21: 593-601. – reference: Sinha JN, Atkinson JM, Schmitt H. Effects of clonidine and L-dopa on spontaneous and evoked splanchnic nerve discharges. Eur J Pharmacol 1973; 24: 113-119. – reference: Haxhiu MA, Dreshaj I, Schäfer SG, Ernsberger P. Selective antihypertensive action of moxonidine is mediated mainly by I1-imidazoline receptors in the rostral ventrolateral medulla. J Cardiovasc Pharmacol 1994; 24(Suppl. 1): S1-S8. – reference: Onrot J, Goldberg MR, Biaggioni I, Hollister AS, Kincaid D, Robertson D. Postjunctional vascular smooth muscle alpha-2 adrenoreceptors in human autonomic failure. Clin Invest Med 1987; 10: 26-31. – reference: Prichard BN, Graham BR. The use of moxonidine in the treatment of hypertension. J Hypertens Suppl 1997; 15: S47-S55. – reference: Bricca G, Dontenwill M, Molines A, Feldman J, Belcourt A, Bousquet P. The imidazoline preferring receptor: binding studies in bovine, rat and human brain stem. Eur J Pharmacol 1989; 162: 1-9. – reference: Nurnberger J, Dammer S, Mitchell A, et al. Effect of the C825T polymorphism of the G protein beta3 subunit on the systolic blood pressure-lowering effect of clonidine in young, healthy male subjects. Clin Pharmacol Ther 2003; 74: 53-60. – reference: da Costa DF, Bannister R, Landon J, Mathias CJ. Growth hormone response to clonidine is impaired in patients with central sympathetic degeneration. Clin Exp Hypertens A 1984; 6: 1843-1846. – reference: Mukaddam-Daher S, Lambert C, Gutkowska J. Clonidine and ST-91 may activate imidazoline binding sites in the heart to release atrial natriuretic peptide. Hypertension 1997; 30: 83-87. – reference: Thomaides TN, Chaudhuri KR, Maule S, Watson L, Marsden CD, Mathias CJ. Growth hormone response to clonidine in central and peripheral primary autonomic failure. Lancet 1992; 340: 263-266. – reference: Robertson D, Goldberg MR, Tung CS, Hollister AS, Robertson RM. Use of alpha 2 adrenoreceptor agonists and antagonists in the functional assessment of the sympathetic nervous system. J Clin Invest 1986; 78: 576-581. – reference: Reid JL, Wing LM, Mathias CJ, Frankel HL, Neill E. The central hypotensive effect of clonidine. Studies in tetraplegic subjects. Clin Pharmacol Ther 1977; 21: 375-381. – reference: Smedes F, Kraak JC, Poppe H. A simple and fast solvent extraction system for selective and quantitative isolation of adrenaline, noradrenaline and dopamine from plasma and urine. J Chromatogr 1982; 231: 25-39. – reference: Isaac L. Brain sites for the antihypertensive effects of clonidine. Prog Clin Biol Res 1981; 71: 29-39. – reference: Khan ZP, Ferguson CN, Jones RM. Alpha-2 and imidazoline receptor agonists. Anaesthesia 1999; 54: 146-165. – reference: Zoukos Y, Thomaides T, Pavitt DV, Cuzner ML, Mathias CJ. Beta-adrenoceptor expression on circulating mononuclear cells of idiopathic Parkinson's disease and autonomic failure patients before and after reduction of central sympathetic outflow by clonidine. Neurology 1993; 43: 1181-1187. – reference: Tsai ML, Lin MT. Participation of a bulbospinal serotonergic pathway in the rat brain in clonidine-induced hypotension and bradycardia. Pharmacology 1987; 35: 279-285. – reference: Kimber JR, Watson L, Mathias CJ. Distinction of idiopathic Parkinson's disease from multiple system atrophy by stimulation of growth hormone release with clonidine. Lancet 1997; 349: 1877-1881. – reference: Kiowski W, Hulthen UL, Ritz R, Buhler FR. Alpha-2 adrenoceptor-mediated vasoconstriction of arteries. Clin Pharmacol Ther 1983; 34: 365-369. – reference: Senard JM, Arias A, Berlan M, Tran MA, Rascol A, Montastruc JL. Pharmacological evidence of alpha 1- and alpha 2-adrenergic supersensitivity in orthostatic hypotension due to spinal cord injury: a case report. Eur J Clin Pharmacol 1991; 41: 593-596. – volume: 75 start-page: 71 year: 1988 end-page: 77 article-title: Intravenous morphine causes hypertension, hyperglycaemia and increases sympatho‐adrenal outflow in conscious rabbits publication-title: Clin Sci – volume: 71 start-page: 29 year: 1981 end-page: 39 article-title: Brain sites for the antihypertensive effects of clonidine publication-title: Prog Clin Biol Res – volume: 11 start-page: 128 year: 2001 end-page: 135 article-title: Age‐ and gender‐related growth hormone responses to intravenous clonidine in healthy adults publication-title: Growth Horm IGF Res – volume: 78 start-page: 576 year: 1986 end-page: 581 article-title: Use of alpha 2 adrenoreceptor agonists and antagonists in the functional assessment of the sympathetic nervous system publication-title: J Clin Invest – start-page: 232 year: 2002 end-page: 244 – volume: 82 start-page: 627 year: 1996 end-page: 635 article-title: Intrathecal clonidine and tizanidine in conscious dogs: comparison of analgesic and hemodynamic effects publication-title: Anesth Analg – volume: 57 start-page: 449P year: 1976 end-page: 450P article-title: The cardiovascular effects of clonidine in rabbits after cervical spinal cord transection publication-title: Br J Pharmacol – volume: 10 start-page: 26 year: 1987 end-page: 31 article-title: Postjunctional vascular smooth muscle alpha‐2 adrenoreceptors in human autonomic failure publication-title: Clin Invest Med – volume: 43 start-page: 1181 year: 1993 end-page: 1187 article-title: Beta‐adrenoceptor expression on circulating mononuclear cells of idiopathic Parkinson's disease and autonomic failure patients before and after reduction of central sympathetic outflow by clonidine publication-title: Neurology – volume: 319 start-page: 69 year: 1984 end-page: 101 article-title: Distribution of alpha 2 agonist binding sites in the rat and human central nervous system: analysis of some functional, anatomic correlates of the pharmacologic effects of clonidine and related adrenergic agents publication-title: Brain Res – volume: 35 start-page: 279 year: 1987 end-page: 285 article-title: Participation of a bulbospinal serotonergic pathway in the rat brain in clonidine‐induced hypotension and bradycardia publication-title: Pharmacology – volume: 231 start-page: 25 year: 1982 end-page: 39 article-title: A simple and fast solvent extraction system for selective and quantitative isolation of adrenaline, noradrenaline and dopamine from plasma and urine publication-title: J Chromatogr – volume: 109 start-page: 21 year: 2003 end-page: 28 article-title: Blockade of N‐methyl‐D‐aspartate receptors within the rostral ventrolateral medulla antagonizes clonidine‐induced cardiovascular effects publication-title: Auton Neurosci – volume: 21 start-page: 375 year: 1977 end-page: 381 article-title: The central hypotensive effect of clonidine. Studies in tetraplegic subjects publication-title: Clin Pharmacol Ther – volume: 46 start-page: 103 year: 1989 end-page: 109 article-title: Assessment of MK‐912, an α ‐adrenoceptor antagonist, with use of intravenous clonidine publication-title: Clin Pharmacol Ther – volume: 162 start-page: 1 year: 1989 end-page: 9 article-title: The imidazoline preferring receptor: binding studies in bovine, rat and human brain stem publication-title: Eur J Pharmacol – volume: 54 start-page: 146 year: 1999 end-page: 165 article-title: Alpha‐2 and imidazoline receptor agonists publication-title: Anaesthesia – volume: 15 start-page: S47 issue: Suppl year: 1997 end-page: S55 article-title: The use of moxonidine in the treatment of hypertension publication-title: J Hypertens – volume: 422 start-page: 336 year: 1987 end-page: 346 article-title: Ventrolateral medullary pressor area: site of hypotensive action of clonidine publication-title: Brain Res – volume: 34 start-page: 1012 year: 1999 end-page: 1015 article-title: Cardiovascular effects of clonidine‐like drugs in pithed rabbits publication-title: Hypertension – volume: 74 start-page: 53 year: 2003 end-page: 60 article-title: Effect of the C825T polymorphism of the G protein beta3 subunit on the systolic blood pressure‐lowering effect of clonidine in young, healthy male subjects publication-title: Clin Pharmacol Ther – volume: 41 start-page: 593 year: 1991 end-page: 596 article-title: Pharmacological evidence of alpha 1‐ and alpha 2‐adrenergic supersensitivity in orthostatic hypotension due to spinal cord injury: a case report publication-title: Eur J Clin Pharmacol – volume: 74 start-page: 189 year: 1998 end-page: 192 article-title: Consensus statement on the diagnosis of multiple system atrophy publication-title: J Auton Nerv Syst – volume: 340 start-page: 263 year: 1992 end-page: 266 article-title: Growth hormone response to clonidine in central and peripheral primary autonomic failure publication-title: Lancet – volume: 349 start-page: 1877 year: 1997 end-page: 1881 article-title: Distinction of idiopathic Parkinson's disease from multiple system atrophy by stimulation of growth hormone release with clonidine publication-title: Lancet – volume: 24 start-page: S1 issue: Suppl. 1 year: 1994 end-page: S8 article-title: Selective antihypertensive action of moxonidine is mediated mainly by I ‐imidazoline receptors in the rostral ventrolateral medulla publication-title: J Cardiovasc Pharmacol – year: 2004 – volume: 6 start-page: 1843 year: 1984 end-page: 1846 article-title: Growth hormone response to clonidine is impaired in patients with central sympathetic degeneration publication-title: Clin Exp Hypertens A – volume: 24 start-page: 113 year: 1973 end-page: 119 article-title: Effects of clonidine and ‐dopa on spontaneous and evoked splanchnic nerve discharges publication-title: Eur J Pharmacol – volume: 21 start-page: 593 year: 1977 end-page: 601 article-title: Pharmacokinetics and concentration‐effects of intravenous and oral clonidine publication-title: Clin Pharmacol Ther – volume: 34 start-page: 75 year: 1991 end-page: 83 article-title: Haemodynamic and neurohormonal effects of clonidine in patients with preganglionic and postganglionic sympathetic lesions. Evidence for a central sympatholytic action publication-title: Circulation – volume: 34 start-page: 365 year: 1983 end-page: 369 article-title: Alpha‐2 adrenoceptor‐mediated vasoconstriction of arteries publication-title: Clin Pharmacol Ther – volume: 57 start-page: 425s issue: Suppl. 5 year: 1979 end-page: 428s article-title: Antihypertensive effects of clonidine in tetraplegic subjects devoid of central sympathetic control publication-title: Clin Sci – volume: 30 start-page: 83 year: 1997 end-page: 87 article-title: Clonidine and ST‐91 may activate imidazoline binding sites in the heart to release atrial natriuretic peptide publication-title: Hypertension – volume: 2 start-page: 165 year: 1992 end-page: 170 article-title: Up‐regulation of beta‐adrenoceptors on circulating mononuclear cells after reduction of central sympathetic outflow by clonidine in normal subjects publication-title: Clin Auton Res – volume: 278 start-page: 617 year: 1990 end-page: 633 article-title: Clinical autonomic and therapeutic observations in two siblings with postural hypotension and sympathetic failure due to an inability to synthesize noradrenaline from dopamine because of a deficiency of dopamine beta hydroxylase publication-title: Q J Med – volume: 82 start-page: 627 year: 1996 ident: 10.1002/mds.20755-BIB17 publication-title: Anesth Analg – volume: 15 start-page: s47 year: 1997 ident: 10.1002/mds.20755-BIB22 publication-title: J Hypertens doi: 10.1097/00004872-199715011-00007 – volume: 11 start-page: 128 year: 2001 ident: 10.1002/mds.20755-BIB6 publication-title: Growth Horm IGF Res doi: 10.1054/ghir.2001.0199 – volume: 78 start-page: 576 year: 1986 ident: 10.1002/mds.20755-BIB9 publication-title: J Clin Invest doi: 10.1172/JCI112611 – volume: 74 start-page: 189 year: 1998 ident: 10.1002/mds.20755-BIB11 publication-title: J Auton Nerv Syst – volume: 34 start-page: 1012 year: 1999 ident: 10.1002/mds.20755-BIB32 publication-title: Hypertension doi: 10.1161/01.HYP.34.4.1012 – volume: 57 start-page: 449p year: 1976 ident: 10.1002/mds.20755-BIB36 publication-title: Br J Pharmacol – volume: 349 start-page: 1877 year: 1997 ident: 10.1002/mds.20755-BIB10 publication-title: Lancet doi: 10.1016/S0140-6736(96)10168-9 – volume: 21 start-page: 593 year: 1977 ident: 10.1002/mds.20755-BIB16 publication-title: Clin Pharmacol Ther doi: 10.1002/cpt1977215593 – volume: 162 start-page: 1 year: 1989 ident: 10.1002/mds.20755-BIB23 publication-title: Eur J Pharmacol doi: 10.1016/0014-2999(89)90597-9 – volume: 24 start-page: s1 year: 1994 ident: 10.1002/mds.20755-BIB24 publication-title: J Cardiovasc Pharmacol doi: 10.1097/00005344-199424001-00002 – volume: 319 start-page: 69 year: 1984 ident: 10.1002/mds.20755-BIB30 publication-title: Brain Res doi: 10.1016/0165-0173(84)90030-4 – volume: 54 start-page: 146 year: 1999 ident: 10.1002/mds.20755-BIB7 publication-title: Anaesthesia doi: 10.1046/j.1365-2044.1999.00659.x – volume-title: Neurology in clinical practice year: 2004 ident: 10.1002/mds.20755-BIB12 – volume: 2 start-page: 165 year: 1992 ident: 10.1002/mds.20755-BIB5 publication-title: Clin Auton Res doi: 10.1007/BF01818957 – volume: 57 start-page: 425s year: 1979 ident: 10.1002/mds.20755-BIB31 publication-title: Clin Sci doi: 10.1042/cs057425s – volume: 422 start-page: 336 year: 1987 ident: 10.1002/mds.20755-BIB20 publication-title: Brain Res doi: 10.1016/0006-8993(87)90941-3 – volume: 109 start-page: 21 year: 2003 ident: 10.1002/mds.20755-BIB21 publication-title: Auton Neurosci doi: 10.1016/j.autneu.2003.08.011 – volume: 10 start-page: 26 year: 1987 ident: 10.1002/mds.20755-BIB33 publication-title: Clin Invest Med – volume: 34 start-page: 75 year: 1991 ident: 10.1002/mds.20755-BIB4 publication-title: Circulation doi: 10.1161/01.CIR.84.1.75 – volume: 278 start-page: 617 year: 1990 ident: 10.1002/mds.20755-BIB15 publication-title: Q J Med – volume: 74 start-page: 53 year: 2003 ident: 10.1002/mds.20755-BIB18 publication-title: Clin Pharmacol Ther doi: 10.1016/S0009-9236(03)00087-0 – volume: 340 start-page: 263 year: 1992 ident: 10.1002/mds.20755-BIB1 publication-title: Lancet doi: 10.1016/0140-6736(92)92355-J – volume: 43 start-page: 1181 year: 1993 ident: 10.1002/mds.20755-BIB2 publication-title: Neurology doi: 10.1212/WNL.43.6.1181 – volume: 231 start-page: 25 year: 1982 ident: 10.1002/mds.20755-BIB13 publication-title: J Chromatogr doi: 10.1016/S0378-4347(00)80506-X – volume: 75 start-page: 71 year: 1988 ident: 10.1002/mds.20755-BIB14 publication-title: Clin Sci doi: 10.1042/cs0750071 – volume: 71 start-page: 29 year: 1981 ident: 10.1002/mds.20755-BIB19 publication-title: Prog Clin Biol Res – start-page: 232 volume-title: Autonomic failure: a textbook of clinical disorders of the autonomic nervous system year: 2002 ident: 10.1002/mds.20755-BIB34 – volume: 46 start-page: 103 year: 1989 ident: 10.1002/mds.20755-BIB3 publication-title: Clin Pharmacol Ther doi: 10.1038/clpt.1989.113 – volume: 6 start-page: 1843 year: 1984 ident: 10.1002/mds.20755-BIB8 publication-title: Clin Exp Hypertens A – volume: 35 start-page: 279 year: 1987 ident: 10.1002/mds.20755-BIB25 publication-title: Pharmacology doi: 10.1159/000138321 – volume: 21 start-page: 375 year: 1977 ident: 10.1002/mds.20755-BIB27 publication-title: Clin Pharmacol Ther doi: 10.1002/cpt1977214375 – volume: 34 start-page: 365 year: 1983 ident: 10.1002/mds.20755-BIB28 publication-title: Clin Pharmacol Ther doi: 10.1038/clpt.1983.216 – volume: 24 start-page: 113 year: 1973 ident: 10.1002/mds.20755-BIB29 publication-title: Eur J Pharmacol doi: 10.1016/0014-2999(73)90122-2 – volume: 30 start-page: 83 year: 1997 ident: 10.1002/mds.20755-BIB26 publication-title: Hypertension doi: 10.1161/01.HYP.30.1.83 – volume: 41 start-page: 593 year: 1991 ident: 10.1002/mds.20755-BIB35 publication-title: Eur J Clin Pharmacol doi: 10.1007/BF00314991 |
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| SubjectTerms | Adrenergic alpha-Agonists Adrenergic alpha-Agonists - administration & dosage Autonomic Nervous System Diseases Autonomic Nervous System Diseases - blood Autonomic Nervous System Diseases - drug therapy Autonomic Nervous System Diseases - physiopathology Biological and medical sciences Blood Pressure Blood Pressure - drug effects Case-Control Studies Clonidine Clonidine - administration & dosage Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Heart Rate Heart Rate - drug effects Hemodynamics Hemodynamics - drug effects Humans Medical sciences Multiple sclerosis and variants. Guillain barré syndrome and other inflammatory polyneuropathies. Leukoencephalitis Multiple System Atrophy Multiple System Atrophy - blood Multiple System Atrophy - drug therapy Multiple System Atrophy - physiopathology Neurology Norepinephrine Norepinephrine - blood pure autonomic failure Retrospective Studies Statistics, Nonparametric Time Factors |
| Title | Hemodynamic effects of clonidine in two contrasting models of autonomic failure: Multiple system atrophy and pure autonomic failure |
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