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Abstract Injections of the thromboxane A 2 mimetic U-46619 (10 and 20 μg) into the left atrium of anesthetized rabbits evoked decreases in heart rate (HR) and arterial blood pressure (ABP) followed by an increase in ABP. Bilateral, cervical vagotomy abolished the U-46619-induced bradycardia and attenuated the hypotension. Injections of U-46619 into the ascending aorta did not evoke the bradycardia and hypotension but did cause arterial hypertension. To further define the origin of the vagal reflex, recordings of nerve impulses were made from 11 chemosensitive cardiac vagal afferent nerves. Impulse frequency increased in all 11 fibers in response to left atrial injections of phenylbiguanide (20–30 μg) and U-46619 (5–10 μg). Onset time of nerve activity induced by U-46619 correlated with the onset time of bradycardia. We conclude that U-46619 injections into the left heart elicit decreases in HR and ABP via a vagal reflex that originates from the heart similar to the coronary chemoreflex described for other agents. coronary chemoreflex phenylbiguanide prostaglandins anesthetized rabbits Footnotes This work was supported by Grant-in-Aid 0051148Z from the American Heart Association, Heartland Affiliate. Address for reprint requests and other correspondence: J. Orr, Dept. of Molecular Biosciences, 2045 Haworth Hall, Univ. of Kansas, Lawrence, KS 66045 (E-mail: jorr@ku.edu ). The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked “ advertisement ” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact. 10.1152/ajpheart.00624.2001 Copyright © 2002 the American Physiological Society
AJP - Heart and Circulatory Physiology – The American Physiological Society
Published: Feb 1, 2002
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