Prostanoids and cardiac reflexes of sympathetic and vagal origin.
Prostaglandins in concentrations too low to stimulate afferent nerve endings in the heart may sensitize them to chemical or mechanical stimuli that activate cardiac reflexes during myocardial ischemia. Bradykinin, which is released from the heart during ischemia, elicits sympathetically mediated reflex pressor effects and tachycardia when applied in low doses (0.1 to 1 microgram) to the epicardium of the left ventricle in open-chest, anesthetized dogs. The reflex pressor effects evoked by bradykinin are reduced after inhibition of prostaglandins biosynthesis with indomethacin and potentiated by concomitant topical application of low doses (0.1 to 0.3 microgram/min) of PGE1 or PGE2 and prostacyclin (PGI2). The pressor and tachycardic responses to bradykinin are also enhanced after temporary (10-minute) coronary occlusion; this potentiation is abolished by indomethacin treatment and can be restored by superfusing the ventricle with prostaglandins. Nicotine is known to excite mechanosensitive vagal receptors with afferent C fibers, which supply the left ventricle, and to elicit reflex hypotension and bradycardia. This depressor vagal reflex evoked by epicardial or intracoronary administration of nicotine (10 to 50 micrograms) was not affected by either indomethacin or by topical application of PGE1, PGE2, or PGI2. Also, intracoronary infusion of PGE2 (0.1 to 0.3 microgram/min), which enhanced the pressor reflex effects of bradykinin, was without effect on nicotine-induced depressor reflex. However, intracoronary infusion of PGI2 (0.1 to 0.3 microgram/min) significantly enhanced the hypotensive and bradycardic responses to nicotine and, at the same time, reduced sympathetically mediated reflex effects of bradykinin. The hypotensive effects induced by epicardial or intracoronary administration of nicotine were also significantly enhanced during intravenous infusion of subdepressor doses of PGI2 (5 to 20 ng/kg/min). Treatment with captopril, which enhances the endogenous production of prostaglandins, greatly enhanced the reflex depressor effects of nicotine; this potentiating effect of captopril was completely abolished by indomethacin treatment. An increase in the magnitude of nicotine-induced reflex depressor effects was also observed after intravenous injection (1 microgram/kg) or infusion (25 to 50 ng/kg/min) of prostaglandin D2. A working hypothesis is proposed to account for the role of prostanoids in activation of cardiac reflexes during myocardial ischemia.
D001158:Arteries / Q000294:innervation / Q000502:physiology / Q000503:physiopathology; D003327:Coronary Disease / Q000503:physiopathology; D011464:Epoprostenol / Q000502:physiology*; D006321:Heart / Q000294:innervation* / Q000502:physiology / Q000503:physiopathology; D006801:Humans; D008954:Models, Biological; D011311:Pressoreceptors / Q000502:physiology / Q000503:physiopathology; D011453:Prostaglandins / Q000502:physiology*; D012018:Reflex / Q000502:physiology*; D013564:Sympathetic Nervous System / Q000502:physiology* / Q000503:physiopathology; D014630:Vagus Nerve / Q000502:physiology* / Q000503:physiopathology
D011453:Prostaglandins; D011464:Epoprostenol