Key result
Administration of the 5-HT3 antagonist tropisetron attenuated the decreases in heart rate and arterial blood pressure induced by the thromboxane A2 mimetic U-46619 in rabbits.
Supports serotonergic mediation of thromboxane responses; leaves open clinical relevance of 5-HT3 antagonism in humans.
We reported previously that the thromboxane A(2) (TxA(2)) 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 TxA(2) evokes these changes via the release of serotonin [5-hydroxytryptamine (5-HT)] and activation of the 5-HT(3) receptor. Injections of the 5-HT(3) antagonist tropisetron (1 mg of 3-tropanyl-indole-3-carboxylate or ICS-205-930) attenuated the decreases in HR and ABP induced by left atrial injections of U-46619 (20 microg). 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 5-HT and stimulation of the 5-HT(3) receptor plays a significant role in coronary reflexes induced by TxA(2).
No takes yet. Share an insight, caveat, or question.
Wacker et al. (2003) studied this question. Tropisetron (5-HT3 antagonist) was evaluated on Changes in heart rate and arterial blood pressure. Administration of the 5-HT3 antagonist tropisetron attenuated the decreases in heart rate and arterial blood pressure induced by the thromboxane A2 mimetic U-46619 in rabbits.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: