Donate Help Contact The AHA Sign In Home
American Heart Association
Circulation Research
Search: search_blue_button Advanced Search
Circulation Research. 1988;62:891-895

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Young, M. A.
Right arrow Articles by Vatner, S. F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Young, M. A.
Right arrow Articles by Vatner, S. F.

Circulation Research, Vol 62, 891-895, Copyright © 1988 by American Heart Association


ARTICLES

Parasympathetic coronary vasoconstriction induced by nicotine in conscious calves

MA Young, DR Knight and SF Vatner
Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.

We studied the effects of intracoronary injection of nicotine and acetylcholine on coronary blood flow in nine conscious calves chronically instrumented to measure coronary blood flow, left ventricular (LV) and mean arterial pressure, LV dP/dt, and heart rate. Nicotine (5 micrograms/kg i.c.) elicited a biphasic response in coronary blood flow consisting of an initial vasoconstriction (phase 1; blood flow fell by 52 +/- 5.4% from a baseline of 66 +/- 7.5 ml/min) followed by vasodilation (phase 2, blood flow rose 119 +/- 12.7% above baseline). The change in coronary blood flow with nicotine was not associated with changes in LV systolic pressure, mean arterial pressure, or heart rate. The change in coronary blood flow was unaffected by combined alpha- and beta-adrenoceptor blockade with prazosin, rauwolscine, and propranolol but was abolished by either muscarinic blockade with atropine or ganglionic blockade with hexamethonium. Acetylcholine (0.5 microgram/kg i.c.), without affecting mean arterial pressure, elicited changes in coronary blood flow similar to those observed with nicotine, producing an initial phase of coronary vasoconstriction (blood flow fell by 71 +/- 4.9%) followed by vasodilation (blood flow rose by 228 +/- 20.7%). Both phases of the response to acetylcholine were abolished by muscarinic blockade but were unaffected by ganglionic blockade. When nicotine was injected into the left circumflex coronary artery, no change in blood flow was observed in the left anterior descending coronary artery, indicating the lack of involvement of global reflex pathways. These results suggest that nicotine locally stimulates parasympathetic nerves, which constrict the coronary circulation via a muscarinic mechanism.


This article has been cited by other articles:


Home page
J. Pharmacol. Exp. Ther.Home page
Y. Zhang and D. B. Hoover
Signaling Mechanisms for Muscarinic Receptor-Mediated Coronary Vasoconstriction in Isolated Rat Hearts
J. Pharmacol. Exp. Ther., April 1, 2000; 293(1): 96 - 106.
[Abstract] [Full Text]