| Relaxant effect of C-type natriuretic peptide involves endothelium and nitric oxide-cGMP system in rat coronary microvasculature. | |
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MedLine Citation:
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PMID: 11476748 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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OBJECTIVE: Recent evidence suggests a possible role for nitric oxide (NO) in atrial natriuretic peptide-induced blood pressure effects. We tested the hypothesis that C-type natriuretic peptide (CNP)-mediated relaxation of the rat coronary circulation involves NO and activation of soluble guanylyl cyclase. METHODS: Rat hearts (n=6 per group) were perfused in vitro at constant flow and the effect of CNP (0.1-3 micromol/l) on coronary perfusion pressure (a measure of vascular tone) and release of guanosine 3',5'-cyclic monophosphate (cGMP) was determined in absence and presence of the nitric oxide (NO) synthase inhibitor N(G)-nitro-L-arginine (L-NNA; 0.2 mmol/l) or the natriuretic peptide receptor antagonist HS-142-1 (50 microg/ml). The involvement of Ca(2+)-gated and ATP-dependent K(+) channels in CNP-induced relaxation was tested with iberiotoxin (30 nmol/l) and glibenclamide (1 micromol/l), respectively. Rings of rat aorta (n=12) were tested using the organ bath set-up. RESULTS: CNP reduced perfusion pressure from 134 +/- 2 mmHg (baseline) to 71 +/- 1 mmHg (-48%) and this effect was significantly attenuated by L-NNA (-37%) or HS-142-1 (-19%). In presence of glibenclamide, CNP reduced perfusion pressure to 92 +/- 2 mmHg (-32%), in presence of iberiotoxin to 93 +/- 1 mmHg (-30% and in their combined presence to 102+/-2 mmHg (-23%) (P<0.05 vs. corresponding control). Basal release of cGMP was increased up to 4-fold by CNP and this increase was reduced (-50%) in presence of L-NNA or HS-142-1 (-68%). By contrast, relaxation of rat aortic rings mounted in organ baths was insensitive to inhibition by L-NNA. CONCLUSION: Relaxation of the coronary resistance vessels of the rat by CNP is partly mediated by the NO-cGMP pathway. These novel data support the existence of an endogenous link between soluble and particulate guanylyl cyclases in the control of natriuretic peptide-mediated coronary resistance vessel function. |
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Authors:
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F Brunner; G Wölkart |
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Publication Detail:
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Type: In Vitro; Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Cardiovascular research Volume: 51 ISSN: 0008-6363 ISO Abbreviation: Cardiovasc. Res. Publication Date: 2001 Aug |
Date Detail:
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Created Date: 2001-07-30 Completed Date: 2001-10-04 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 0077427 Medline TA: Cardiovasc Res Country: Netherlands |
Other Details:
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Languages: eng Pagination: 577-84 Citation Subset: IM |
Affiliation:
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Institut für Pharmakologie und Toxikologie, Karl-Franzens-Universität Graz, Universitätsplatz 2, A-8010, Graz, Austria. friedrich.brunner@kfunigraz.ac.at |
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Aorta / drug effects Blood Pressure / drug effects Coronary Vessels / drug effects*, physiology Cyclic GMP / physiology* Dose-Response Relationship, Drug Endothelium, Vascular / drug effects*, physiology Female Male Microcirculation / drug effects Natriuretic Peptide, C-Type / pharmacology* Nitric Oxide / physiology* Nitric Oxide Synthase / antagonists & inhibitors Nitroarginine / pharmacology Organ Culture Techniques Potassium Channels / physiology Rats Rats, Sprague-Dawley Vasodilation / drug effects, physiology |
| Chemical | |
Reg. No./Substance:
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0/Potassium Channels; 10102-43-9/Nitric Oxide; 127869-51-6/Natriuretic Peptide, C-Type; 2149-70-4/Nitroarginine; 7665-99-8/Cyclic GMP; EC 1.14.13.39/Nitric Oxide Synthase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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