Effects of carotid artery occlusion on the pressor response induced by sustained isometric contraction in the cat

• Published in: Cardiovascular research Vol. 21; no. 7; pp. 521 - 529
• Main Authors: SPARKS, DAVID P, PAUL, DANIEL J, WILLIAMS, CAROLE A
• Format: Journal Article
• Language: English
• Published: Oxford Oxford University Press 01.07.1987
• Subjects: Animals; arterial blood pressure; Arterial Occlusive Diseases - physiopathology; baroreceptor reflex; Biological and medical sciences; Blood Pressure - drug effects; Carotid Artery Diseases - physiopathology; Cats; clonidine; Clonidine - pharmacology; Fundamental and applied biological sciences. Psychology; Hemodynamics. Rheology; Isometric Contraction; isometric contractions; Muscle Contraction; Naloxone - pharmacology; Pressoreceptors - physiopathology; Reflex - drug effects; Vertebrates: cardiovascular system; Fissipedia; Carnivora; Vertebrata; Mammalia; Cat; Isometric muscular contraction; Blood pressure; α-Adrenergic receptor agonist; Hemodynamics; Barorreceptor
• DOI: 10.1093/cvr/21.7.521
• ISSN: 0008-6363

The effects of clonidine, a central alpha2 agonist, on changes in blood pressure caused by muscle afferent nerve (ergoreceptor) activation and baroreceptor manipulation were studied in cats. Prolonged isometric contractions (ergoreceptor activation) of the gastrocnemius and plantaris muscles increased mean arterial pressure by 53 mmHg. This pressor response was not altered by naloxone (0.5 μmol·litre−1) but was eliminated by clonidine (0.5-2.0 μg) when injected into the cerebral aqueduct. Brief occlusion of the carotid artery (15-30 s) caused mean arterial pressure to increase by 32-42 mmHg at rest. Neither naloxone nor clonidine altered the magnitude of the reflex pressor response to carotid occlusion. Similar increases in pressure were measured when occlusion was applied during fatiguing isometric contractions; thus baroreceptor induced increases in pressure were superimposed on the ergoreceptor induced blood pressure changes. Naloxone did not affect the changes in pressure caused by either reflex response. Clonidine continued to eliminate the pressor response to muscular contraction but did not affect the pressure increase when the carotid occlusion was applied during contractions. Electrical stimulation of the carotid sinus nerve caused blood pressure to decrease by 36 mmHg during rest and by 41 mmHg during fatiguing isometric contractions. Clonidine did not alter the depressor response to carotid sinus nerve stimulation. These data may indicate that separate pathways centrally mediate the changes in blood pressure caused by ergoreceptor and baroreceptor afferent activation. The integration of the ergoreceptor pathway may involve a catecholaminergic-opioidergic system but the present results do not suggest a similar interaction for the baroreceptor integration.