Document Detail


Intracoronary angiotensin II potentiates coronary sympathetic vasoconstriction in humans.
MedLine Citation:
PMID:  9236429     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: In humans with coronary artery disease, ACE inhibition attenuates coronary sympathetic vasoconstriction. Whether this is due to removal of angiotensin (Ang) II production or to a reduced bradykinin breakdown, however, is unknown. METHODS AND RESULTS: In eight normotensive patients with angiographic evidence of mild left coronary artery lesions (< or = 50%), mean arterial pressure (MAP, intra-arterial catheter), heart rate (HR, ECG lead), coronary sinus blood flow (CBF, thermodilution method), and coronary vascular resistance (CVR, ratio between MAP and CBF) were measured before and during a 15-minute left intracoronary infusion of Ang II at a dose that had no direct coronary or systemic vasomotor effects. The same measurements were made before and during a 15-minute infusion of saline. A 2-minute cold pressor test (CPT) and a 45-second diving were performed at the end of either infusion period. These maneuvers were used because their coronary vasomotor effects are abolished by phentolamine and thus depend on sympathetic activation. During saline infusion, both CPT and diving caused a marked increase in MAP. HR increased with CPT and fell with diving. CBF increased in parallel to the MAP increase, with little change in CVR. The MAP and HR responses were similar during Ang II infusion, which, however, caused either no change or a reduction in CBF with a consequent marked increase in CVR with both CPT and diving. In four additional patients, the diameter of the stenotic vessels remained unchanged during the CPT performed under saline and Ang II infusion. CONCLUSIONS: Ang II markedly enhances sympathetic influences on coronary circulation in humans, presumably by acting at the arteriolar level. This may explain the blunting effect of ACE inhibition on sympathetic coronary vasoconstriction in patients with coronary artery disease.
Authors:
A Saino; G Pomidossi; R Perondi; R Valentini; A Rimini; L Di Francesco; G Mancia
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Publication Detail:
Type:  Clinical Trial; Controlled Clinical Trial; Journal Article    
Journal Detail:
Title:  Circulation     Volume:  96     ISSN:  0009-7322     ISO Abbreviation:  Circulation     Publication Date:  1997 Jul 
Date Detail:
Created Date:  1997-08-14     Completed Date:  1997-08-14     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0147763     Medline TA:  Circulation     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  148-53     Citation Subset:  AIM; IM    
Affiliation:
Centro di Fisiologia Clinica e Ipertensione, Università di Milano, Ospedale Maggiote, Italy.
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MeSH Terms
Descriptor/Qualifier:
Aged
Angiotensin II / pharmacology,  physiology*
Angiotensin-Converting Enzyme Inhibitors / pharmacology,  therapeutic use
Captopril / pharmacology,  therapeutic use
Coronary Angiography
Coronary Disease / drug therapy*,  physiopathology*,  radiography
Coronary Vessels / drug effects,  physiology*
Female
Hemodynamics / drug effects,  physiology
Humans
Infusions, Intravenous
Male
Middle Aged
Vasoconstriction / drug effects,  physiology*
Vasoconstrictor Agents / pharmacology
Chemical
Reg. No./Substance:
0/Angiotensin-Converting Enzyme Inhibitors; 0/Vasoconstrictor Agents; 11128-99-7/Angiotensin II; 62571-86-2/Captopril
Comments/Corrections
Comment In:
Circulation. 1998 May 12;97(18):1873-4   [PMID:  9603547 ]

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


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