Document Detail

Coronary vasodilation to acetylcholine, adenosine and bradykinin in dogs: effects of inhibition of NO-synthesis and captopril.
MedLine Citation:
PMID:  8293769     Owner:  NLM     Status:  MEDLINE    
We investigated the effects of inhibition of both nitric oxide (NO) synthesis and angiotensin converting enzyme (ACE) on agonist-induced relaxations in the coronary system. Chronically instrumented conscious dogs (n = 4) were prepared for the measurement of coronary blood flow (CBF), coronary diameter of the left circumflex artery (LCX), mean arterial blood pressure (MAP) and heart rate (HR). Intracoronary infusions of acetylcholine, adenosine and bradykinin were performed after intracoronary pretreatment of either vehicle, L-NAME (6, captopril (1 or both L-NAME+captopril. Acetylcholine bradykinin and adenosine caused dose-dependent increases in CBF and LCX. HR increased concomitantly. Captopril potentiated the vasodilating effects of bradykinin and acetylcholine on LCX and CBF significantly (P < or = 0.05) and those of adenosine slightly. L-NAME caused vasoconstriction, hypertension and bradycardia. The effects of acetylcholine on CBF were abolished during L-NAME treatment while bradykinin and adenosine responses were markedly reduced. When captopril and L-NAME were given simultaneously, the vasodilator responses to bradykinin but not to acetylcholine or adenosine were partially restored (P < or = 0.05). We conclude that in vivo, (a) adenosine possibly elicits endothelium-dependent dilation; (b) adenosine and bradykinin act in part independently of the L-arginine/NO pathway; (c) vasodilation to acetylcholine is potentiated by acute ACE inhibition via NO-dependent mechanisms.
J Zanzinger; E Bassenge
Related Documents :
1273749 - Shunting, release, and distribution of nine and fifteen micron spheres in myocardium.
15993879 - Effect of prostaglandin i2 analogues on left ventricular diastolic function in vivo.
25492829 - The effect of simvastatin and pravastatin on arterial blood pressure, baroreflex, vasoc...
10790739 - Association of sudden infant death syndrome with grossly deranged iron metabolism and n...
16093919 - Mechanisms of adenosine-induced renal vasodilatation in hypertensive patients.
3748319 - The effects of central injections of adenosine analogs on blood pressure and heart rate...
12208799 - Left ventricular systolic unloading and augmentation of intracoronary pressure and dopp...
10520859 - A pilot study on the hemodynamic effect of short-term ursodeoxycholic acid therapy in p...
22165459 - Comparison of ropivacaine and lidocaine with epinephrine for infiltration anesthesia in...
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  European heart journal     Volume:  14 Suppl I     ISSN:  0195-668X     ISO Abbreviation:  Eur. Heart J.     Publication Date:  1993 Nov 
Date Detail:
Created Date:  1994-03-03     Completed Date:  1994-03-03     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  8006263     Medline TA:  Eur Heart J     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  164-8     Citation Subset:  IM    
Department of Applied Physiology, University of Freiburg, Germany.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Acetylcholine / physiology
Adenosine / physiology
Arginine / analogs & derivatives,  pharmacology
Bradykinin / physiology
Captopril / pharmacology*
Coronary Vessels / drug effects*,  physiology
Drug Synergism
NG-Nitroarginine Methyl Ester
Nitric Oxide / biosynthesis
Vasodilation / drug effects*,  physiology
Reg. No./Substance:
10102-43-9/Nitric Oxide; 50903-99-6/NG-Nitroarginine Methyl Ester; 51-84-3/Acetylcholine; 58-61-7/Adenosine; 58-82-2/Bradykinin; 62571-86-2/Captopril; 74-79-3/Arginine

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  Angiotensin-converting enzyme inhibitors unmask endogenous kinin production by bovine coronary arter...
Next Document:  Modulation of sympathetic control by ACE inhibitors.