Endothelium removal augments endothelium‐independent vasodilatation in rat mesenteric vascular bed
Background and purpose: The vascular endothelium regulates vascular tone by releasing various endothelium‐derived vasoactive substances to counteract excess vascular response. We investigated whether the vascular endothelium regulates vasodilatation via released endothelium‐derived contracting facto...
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| Published in | British journal of pharmacology Vol. 154; no. 1; pp. 32 - 40 |
|---|---|
| Main Authors | , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Oxford, UK
Blackwell Publishing Ltd
01.05.2008
Nature Publishing Nature Publishing Group |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Background and purpose: The vascular endothelium regulates vascular tone by releasing various endothelium‐derived vasoactive substances to counteract excess vascular response. We investigated whether the vascular endothelium regulates vasodilatation via released endothelium‐derived contracting factors (EDCFs), by examining the effect of endothelium removal on responses to periarterial nerve stimulation (PNS) and various vasodilator agents.
Experimental approach: The rat mesenteric vascular bed was perfused with Krebs solution. Vasodilator responses to PNS and 5 min perfusion of vasodilator agents in preparations with endothelium were compared with those in the same preparations without endothelium. The endothelium was removed by 30 s perfusion with sodium deoxycholate.
Key results: Endothelium removal significantly augmented vasodilator responses to PNS and calcitonin gene‐related peptide (CGRP), isoprenaline (β‐adrenoceptor agonist), SNP and 8‐bromo‐cGMP (8‐Br‐cGMP; cGMP analogue) but not BAY41‐2272 (soluble guanylate cyclase activator). The augmentation of SNP‐induced vasodilatation after denudation was much greater than that of CGRP‐ or isoprenaline‐induced vasodilatation. In the preparations with an intact endothelium, L‐NAME (nitric oxide synthase inhibitor) significantly augmented vasodilator responses to PNS and CGRP, isoprenaline, SNP and 8‐Br‐cGMP, but not BAY41‐2272. Indomethacin (cyclooxygenase inhibitor) and seratrodast (thromboxane A2 receptor antagonist), but not phosphoramidon (endothelin‐1‐converting enzyme inhibitor) or BQ‐123 (selective endothelin type A receptor antagonists), significantly augmented vasodilator responses to PNS and CGRP, isoprenaline, SNP and BAY41‐2272.
Conclusion and implication: These results suggest that the endothelium in rat mesenteric arteries regulates and maintains vascular tone via counteracting not only vasoconstriction through releasing endothelium‐derived relaxing factors, but also vasodilatation, in part by releasing an EDCF, thromboxane A2. |
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| AbstractList | The vascular endothelium regulates vascular tone by releasing various endothelium-derived vasoactive substances to counteract excess vascular response. We investigated whether the vascular endothelium regulates vasodilatation via released endothelium-derived contracting factors (EDCFs), by examining the effect of endothelium removal on responses to periarterial nerve stimulation (PNS) and various vasodilator agents.
The rat mesenteric vascular bed was perfused with Krebs solution. Vasodilator responses to PNS and 5 min perfusion of vasodilator agents in preparations with endothelium were compared with those in the same preparations without endothelium. The endothelium was removed by 30 s perfusion with sodium deoxycholate.
Endothelium removal significantly augmented vasodilator responses to PNS and calcitonin gene-related peptide (CGRP), isoprenaline (beta-adrenoceptor agonist), SNP and 8-bromo-cGMP (8-Br-cGMP; cGMP analogue) but not BAY41-2272 (soluble guanylate cyclase activator). The augmentation of SNP-induced vasodilatation after denudation was much greater than that of CGRP- or isoprenaline-induced vasodilatation. In the preparations with an intact endothelium, L-NAME (nitric oxide synthase inhibitor) significantly augmented vasodilator responses to PNS and CGRP, isoprenaline, SNP and 8-Br-cGMP, but not BAY41-2272. Indomethacin (cyclooxygenase inhibitor) and seratrodast (thromboxane A(2) receptor antagonist), but not phosphoramidon (endothelin-1-converting enzyme inhibitor) or BQ-123 (selective endothelin type A receptor antagonists), significantly augmented vasodilator responses to PNS and CGRP, isoprenaline, SNP and BAY41-2272.
These results suggest that the endothelium in rat mesenteric arteries regulates and maintains vascular tone via counteracting not only vasoconstriction through releasing endothelium-derived relaxing factors, but also vasodilatation, in part by releasing an EDCF, thromboxane A(2). Background and purpose: The vascular endothelium regulates vascular tone by releasing various endothelium‐derived vasoactive substances to counteract excess vascular response. We investigated whether the vascular endothelium regulates vasodilatation via released endothelium‐derived contracting factors (EDCFs), by examining the effect of endothelium removal on responses to periarterial nerve stimulation (PNS) and various vasodilator agents. Experimental approach: The rat mesenteric vascular bed was perfused with Krebs solution. Vasodilator responses to PNS and 5 min perfusion of vasodilator agents in preparations with endothelium were compared with those in the same preparations without endothelium. The endothelium was removed by 30 s perfusion with sodium deoxycholate. Key results: Endothelium removal significantly augmented vasodilator responses to PNS and calcitonin gene‐related peptide (CGRP), isoprenaline (β‐adrenoceptor agonist), SNP and 8‐bromo‐cGMP (8‐Br‐cGMP; cGMP analogue) but not BAY41‐2272 (soluble guanylate cyclase activator). The augmentation of SNP‐induced vasodilatation after denudation was much greater than that of CGRP‐ or isoprenaline‐induced vasodilatation. In the preparations with an intact endothelium, L ‐NAME (nitric oxide synthase inhibitor) significantly augmented vasodilator responses to PNS and CGRP, isoprenaline, SNP and 8‐Br‐cGMP, but not BAY41‐2272. Indomethacin (cyclooxygenase inhibitor) and seratrodast (thromboxane A 2 receptor antagonist), but not phosphoramidon (endothelin‐1‐converting enzyme inhibitor) or BQ‐123 (selective endothelin type A receptor antagonists), significantly augmented vasodilator responses to PNS and CGRP, isoprenaline, SNP and BAY41‐2272. Conclusion and implication: These results suggest that the endothelium in rat mesenteric arteries regulates and maintains vascular tone via counteracting not only vasoconstriction through releasing endothelium‐derived relaxing factors, but also vasodilatation, in part by releasing an EDCF, thromboxane A 2 . BACKGROUND AND PURPOSEThe vascular endothelium regulates vascular tone by releasing various endothelium-derived vasoactive substances to counteract excess vascular response. We investigated whether the vascular endothelium regulates vasodilatation via released endothelium-derived contracting factors (EDCFs), by examining the effect of endothelium removal on responses to periarterial nerve stimulation (PNS) and various vasodilator agents. EXPERIMENTAL APPROACHThe rat mesenteric vascular bed was perfused with Krebs solution. Vasodilator responses to PNS and 5 min perfusion of vasodilator agents in preparations with endothelium were compared with those in the same preparations without endothelium. The endothelium was removed by 30 s perfusion with sodium deoxycholate. KEY RESULTSEndothelium removal significantly augmented vasodilator responses to PNS and calcitonin gene-related peptide (CGRP), isoprenaline (beta-adrenoceptor agonist), SNP and 8-bromo-cGMP (8-Br-cGMP; cGMP analogue) but not BAY41-2272 (soluble guanylate cyclase activator). The augmentation of SNP-induced vasodilatation after denudation was much greater than that of CGRP- or isoprenaline-induced vasodilatation. In the preparations with an intact endothelium, L-NAME (nitric oxide synthase inhibitor) significantly augmented vasodilator responses to PNS and CGRP, isoprenaline, SNP and 8-Br-cGMP, but not BAY41-2272. Indomethacin (cyclooxygenase inhibitor) and seratrodast (thromboxane A(2) receptor antagonist), but not phosphoramidon (endothelin-1-converting enzyme inhibitor) or BQ-123 (selective endothelin type A receptor antagonists), significantly augmented vasodilator responses to PNS and CGRP, isoprenaline, SNP and BAY41-2272. CONCLUSION AND IMPLICATIONThese results suggest that the endothelium in rat mesenteric arteries regulates and maintains vascular tone via counteracting not only vasoconstriction through releasing endothelium-derived relaxing factors, but also vasodilatation, in part by releasing an EDCF, thromboxane A(2). Background and purpose: The vascular endothelium regulates vascular tone by releasing various endothelium‐derived vasoactive substances to counteract excess vascular response. We investigated whether the vascular endothelium regulates vasodilatation via released endothelium‐derived contracting factors (EDCFs), by examining the effect of endothelium removal on responses to periarterial nerve stimulation (PNS) and various vasodilator agents. Experimental approach: The rat mesenteric vascular bed was perfused with Krebs solution. Vasodilator responses to PNS and 5 min perfusion of vasodilator agents in preparations with endothelium were compared with those in the same preparations without endothelium. The endothelium was removed by 30 s perfusion with sodium deoxycholate. Key results: Endothelium removal significantly augmented vasodilator responses to PNS and calcitonin gene‐related peptide (CGRP), isoprenaline (β‐adrenoceptor agonist), SNP and 8‐bromo‐cGMP (8‐Br‐cGMP; cGMP analogue) but not BAY41‐2272 (soluble guanylate cyclase activator). The augmentation of SNP‐induced vasodilatation after denudation was much greater than that of CGRP‐ or isoprenaline‐induced vasodilatation. In the preparations with an intact endothelium, L‐NAME (nitric oxide synthase inhibitor) significantly augmented vasodilator responses to PNS and CGRP, isoprenaline, SNP and 8‐Br‐cGMP, but not BAY41‐2272. Indomethacin (cyclooxygenase inhibitor) and seratrodast (thromboxane A2 receptor antagonist), but not phosphoramidon (endothelin‐1‐converting enzyme inhibitor) or BQ‐123 (selective endothelin type A receptor antagonists), significantly augmented vasodilator responses to PNS and CGRP, isoprenaline, SNP and BAY41‐2272. Conclusion and implication: These results suggest that the endothelium in rat mesenteric arteries regulates and maintains vascular tone via counteracting not only vasoconstriction through releasing endothelium‐derived relaxing factors, but also vasodilatation, in part by releasing an EDCF, thromboxane A2. BACKGROUND AND PURPOSE: The vascular endothelium regulates vascular tone by releasing various endothelium-derived vasoactive substances to counteract excess vascular response. We investigated whether the vascular endothelium regulates vasodilatation via released endothelium-derived contracting factors (EDCFs), by examining the effect of endothelium removal on responses to periarterial nerve stimulation (PNS) and various vasodilator agents. EXPERIMENTAL APPROACH: The rat mesenteric vascular bed was perfused with Krebs solution. Vasodilator responses to PNS and 5 min perfusion of vasodilator agents in preparations with endothelium were compared with those in the same preparations without endothelium. The endothelium was removed by 30 s perfusion with sodium deoxycholate. KEY RESULTS: Endothelium removal significantly augmented vasodilator responses to PNS and calcitonin gene-related peptide (CGRP), isoprenaline (beta-adrenoceptor agonist), SNP and 8-bromo-cGMP (8-Br-cGMP; cGMP analogue) but not BAY41-2272 (soluble guanylate cyclase activator). The augmentation of SNP-induced vasodilatation after denudation was much greater than that of CGRP- or isoprenaline-induced vasodilatation. In the preparations with an intact endothelium, L-NAME (nitric oxide synthase inhibitor) significantly augmented vasodilator responses to PNS and CGRP, isoprenaline, SNP and 8-Br-cGMP, but not BAY41-2272. Indomethacin (cyclooxygenase inhibitor) and seratrodast (thromboxane A(2) receptor antagonist), but not phosphoramidon (endothelin-1-converting enzyme inhibitor) or BQ-123 (selective endothelin type A receptor antagonists), significantly augmented vasodilator responses to PNS and CGRP, isoprenaline, SNP and BAY41-2272. CONCLUSION AND IMPLICATION: These results suggest that the endothelium in rat mesenteric arteries regulates and maintains vascular tone via counteracting not only vasoconstriction through releasing endothelium-derived relaxing factors, but also vasodilatation, in part by releasing an EDCF, thromboxane A(2). |
| Author | Iwatani, Y Kosugi, K Isobe‐Oku, S Kawasaki, H Kitamura, Y Atagi, S |
| AuthorAffiliation | 1 Department of Clinical Pharmaceutical Science, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Okayama, Japan 2 Department of Pharmaceutical Care and Health Science, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Okayama, Japan |
| AuthorAffiliation_xml | – name: 1 Department of Clinical Pharmaceutical Science, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Okayama, Japan – name: 2 Department of Pharmaceutical Care and Health Science, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Okayama, Japan |
| Author_xml | – sequence: 1 givenname: Y surname: Iwatani fullname: Iwatani, Y – sequence: 2 givenname: K surname: Kosugi fullname: Kosugi, K – sequence: 3 givenname: S surname: Isobe‐Oku fullname: Isobe‐Oku, S – sequence: 4 givenname: S surname: Atagi fullname: Atagi, S – sequence: 5 givenname: Y surname: Kitamura fullname: Kitamura, Y – sequence: 6 givenname: H surname: Kawasaki fullname: Kawasaki, H |
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| Keywords | Agonist Isoprenaline endothelium-derived contracting factor Vasodilator agent Rat β2-Adrenergic receptor β-Adrenergic receptor agonist Stimulation Neuropeptide Vasodilation β-Adrenergic receptor vasodilatation Vasomotricity Endothelium derived relaxing factor Endothelium derived contracting factor Bronchodilator Rodentia calcitonin gene-related peptide Calcitonin gene related peptide vascular endothelium removal Endothelium Sodium nitroprusside Vertebrata Mammalia periarterial nerve stimulation Animal Antihypertensive agent endothelium-derived relaxing factor |
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| Snippet | Background and purpose: The vascular endothelium regulates vascular tone by releasing various endothelium‐derived vasoactive substances to counteract excess... The vascular endothelium regulates vascular tone by releasing various endothelium-derived vasoactive substances to counteract excess vascular response. We... Background and purpose: The vascular endothelium regulates vascular tone by releasing various endothelium‐derived vasoactive substances to counteract excess... BACKGROUND AND PURPOSE: The vascular endothelium regulates vascular tone by releasing various endothelium-derived vasoactive substances to counteract excess... BACKGROUND AND PURPOSEThe vascular endothelium regulates vascular tone by releasing various endothelium-derived vasoactive substances to counteract excess... |
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| SubjectTerms | Adenylyl Cyclases - metabolism Adrenergic beta-Agonists - pharmacology Animals Biological and medical sciences Calcitonin Gene-Related Peptide - metabolism Calcitonin Gene-Related Peptide - pharmacology calcitonin gene‐related peptide Cyclic AMP - metabolism Cyclic GMP - analogs & derivatives Cyclic GMP - pharmacology Electric Stimulation Endothelium, Vascular - physiology endothelium‐derived contracting factor endothelium‐derived relaxing factor Enzyme Inhibitors - pharmacology Guanylate Cyclase - metabolism isoprenaline Isoproterenol - pharmacology Male Medical sciences NG-Nitroarginine Methyl Ester - pharmacology Nitric Oxide Synthase Type III - antagonists & inhibitors Nitroprusside - pharmacology Perfusion periarterial nerve stimulation Peripheral Nervous System - physiology Pharmacology. Drug treatments Pyrazoles - pharmacology Pyridines - pharmacology Rats Rats, Wistar Receptors, Calcitonin Gene-Related Peptide - drug effects Research Papers sodium nitroprusside Splanchnic Circulation - physiology vascular endothelium removal vasodilatation Vasodilation - physiology Vasodilator Agents - pharmacology |
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| Title | Endothelium removal augments endothelium‐independent vasodilatation in rat mesenteric vascular bed |
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