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Am J Physiol Heart Circ Physiol (October 31, 2002). doi:10.1152/ajpheart.00617.2002
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Articles in PresS, published online ahead of print October 31, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00617.2002
Submitted on July 18, 2002
Accepted on October 30, 2002

The role of serotonin in the thromboxane A2-induced coronary chemoreflex

Michael J. Wacker1*, Heather L. Wilhelm1, Suzanne E. Gomez1, Eric Floor1, and James A. Orr1

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

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

We have reported previously that the thromboxane A2 (TxA2) mimetic, U-46619, stimulates cardiac vagal afferent nerves, eliciting a reflex decrease in heart rate (HR) and arterial blood pressure (ABP). The present experiments were designed to test the hypothesis that thromboxane A2 (TxA2) evokes these changes via the release of serotonin (5-HT) and activation of the 5-HT3 receptor. Injections of the 5-HT3 antagonist, tropisetron (1 mg), attenuated the decreases in HR and ABP induced by left atrial injections of U-46619 (20 µg). Tropisetron administration also eliminated the U-46619 induced increase in impulse frequency in a majority of cardiac, vagal afferent units tested. Measurement of serum 5-HT levels revealed an elevation in serum 5-HT levels after U-46619 injection in those rabbits that displayed a significant HR change following injection of U-46619. These results indicate that although other factors may also contribute to these reflex responses, the release of serotonin and stimulation of the 5-HT3 receptor plays a significant role in coronary reflexes induced by TxA2.




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