Document Detail

Relaxant effect of C-type natriuretic peptide involves endothelium and nitric oxide-cGMP system in rat coronary microvasculature.
MedLine Citation:
PMID:  11476748     Owner:  NLM     Status:  MEDLINE    
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.
F Brunner; G Wölkart
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Cardiovascular research     Volume:  51     ISSN:  0008-6363     ISO Abbreviation:  Cardiovasc. Res.     Publication Date:  2001 Aug 
Date Detail:
Created Date:  2001-07-30     Completed Date:  2001-10-04     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0077427     Medline TA:  Cardiovasc Res     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  577-84     Citation Subset:  IM    
Institut für Pharmakologie und Toxikologie, Karl-Franzens-Universität Graz, Universitätsplatz 2, A-8010, Graz, Austria.
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MeSH Terms
Aorta / drug effects
Blood Pressure / drug effects
Coronary Vessels / drug effects*,  physiology
Cyclic GMP / physiology*
Dose-Response Relationship, Drug
Endothelium, Vascular / drug effects*,  physiology
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, Sprague-Dawley
Vasodilation / drug effects,  physiology
Reg. No./Substance:
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 Oxide Synthase

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