Document Detail


Coronary and systemic hemodynamic effects of sustained inhibition of nitric oxide synthesis in conscious dogs. Evidence for cross talk between nitric oxide and cyclooxygenase in coronary vessels.
MedLine Citation:
PMID:  8756014     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Sustained inhibition of NO synthesis (N omega-nitro-L-arginine [L-NNA], 20 mg.kg-1.d-1, 7 days) was investigated at rest and during exercise in conscious dogs. At rest, L-NNA did not alter mean arterial blood pressure but markedly increased total peripheral resistance (+73 +/- 14%, P < .01). Exaggerated hypertension was observed during exercise (+132 +/- 5 mm Hg after L-NNA versus +113 +/- 5 mm Hg before L-NNA, P < .01). L-NNA decreased the resting coronary artery diameter by 6 +/- 1% and suppressed its exercise-induced dilation but had no effect on coronary blood flow and resistance. L-NNA decreased flow repayment volumes during reactive hyperemia, but corresponding flow debt volumes remained unchanged. The cyclooxygenase inhibitor diclofenac (10 mg/kg) had no effect on reactive hyperemia parameters before L-NNA but reduced flow repayment volumes, durations, and corresponding debt-to-repayment ratios in L-NNA-treated dogs (all P < .05). In vitro, indomethacin blunted the residual relaxation to bradykinin of large coronary arteries taken from L-NNA-treated, but not from control, dogs. Bradykinin-induced increase in 6-ketoprostaglandin F1 alpha production was greater in coronary arteries taken from L-NNA-treated dogs (+ 179 +/- 41 pg/mm2) than from control dogs (+ 66 +/- 18 pg/mm2) (P < .05). These results indicate that (1) NO is of major importance in the control of systemic but not coronary resistance vessels at rest and during exercise, and (2) after L-NNA, the cyclooxygenase pathway is involved in myocardial reactive hyperemia and in the residual relaxation to bradykinin of isolated coronary arteries. Thus, in conscious dogs, the cyclooxygenase pathway might act as a protective mechanism of the coronary circulation when endothelial nitric oxide synthesis is altered.
Authors:
L Puybasset; M L Béa; B Ghaleh; J F Giudicelli; A Berdeaux
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Circulation research     Volume:  79     ISSN:  0009-7330     ISO Abbreviation:  Circ. Res.     Publication Date:  1996 Aug 
Date Detail:
Created Date:  1996-12-12     Completed Date:  1996-12-12     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  0047103     Medline TA:  Circ Res     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  343-57     Citation Subset:  IM    
Affiliation:
Département de Pharmacologie, Faculté de Médecine, Paris-Sud, France.
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MeSH Terms
Descriptor/Qualifier:
Acetylcholine / pharmacology
Animals
Bradykinin / pharmacology
Coronary Circulation / physiology*
Coronary Vessels / physiology*
Diclofenac / pharmacology
Dogs
Epoprostenol / biosynthesis
Femoral Artery / drug effects
Hemodynamics / drug effects,  physiology*
Hyperemia / physiopathology
Nitric Oxide / physiology*
Nitric Oxide Synthase / antagonists & inhibitors
Nitroarginine / pharmacology
Physical Exertion
Prostaglandin-Endoperoxide Synthases / physiology*
Chemical
Reg. No./Substance:
10102-43-9/Nitric Oxide; 15307-86-5/Diclofenac; 2149-70-4/Nitroarginine; 35121-78-9/Epoprostenol; 51-84-3/Acetylcholine; 58-82-2/Bradykinin; EC 1.14.13.39/Nitric Oxide Synthase; EC 1.14.99.1/Prostaglandin-Endoperoxide Synthases

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