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Am J Physiol Heart Circ Physiol (October 18, 2001). doi:10.1152/ajpheart.00624.2001
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Articles in PresS, published online ahead of print October 16, 2001
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00624.2001
Submitted on July 18, 2001
Accepted on October 16, 2001

Thromboxane A2 mimetic evokes a bradycardia mediated by stimulation of cardiac vagal afferent nerves

Michael J Wacker1, Roya N Tehrani1, Rory L Smoot1, and James A Orr1*

1 Molecular Biosciences, University of Kansas, Lawrence, Kansas, USA

* To whom correspondence should be addressed. E-mail: mjwacker{at}eagle.cc.ukans.edu.

Injections of the thromboxane A2 (TXA2) mimetic, U46,619 (10, 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 U46,619-induced bradycardia and attenuated the hypotension. Injections of U46,619 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 cardiac, chemosensitive, vagal, afferent nerves. Impulse frequency increased in all 11 fibers in response to left atrial injections of PBG (20-30 µg) and U46,619 (5-10 µg). The onset time of nerve activity induced by U46,619 correlated with the onset time of the bradycardia. We conclude that U46,619 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.




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