Intracoronary infusion of prostaglandin I₂ attenuates arterial baroreflex control of heart rate in conscious dogs

Prostaglandin I₂ (PGI₂) is known to stimulate ventricular C fiber receptors resulting in a Bezold-Jarisch-like reflex. Also, cardiac receptor stimulation is known to interact with the expression of arterial baroreflexes. Therefore, experiments were performed to determine the effects of left circumflex coronary artery infusion of PGI₂ on the baroreflex control of heart rate in conscious instrumented dogs. Dogs were instrumented chronically with an aortic catheter for the measurement of mean aortic pressure, hydraulic occluder cuffs on the descending aorta and inferior vena cava, a left ventricular catheter for the measurement of left ventricular pressure and heart rate, and a nonocclusive catheter in the left circumflex coronary artery. At the time of experimentation, arterial pressure was altered randomly in steps by partially inflating the occluders. Mean arterial pressure-heart curves (baroflex curves) were constructed by fitting the data to a logistic curve by nonlinear regression. PGI₂ infused into the left circumflex coronary artery at doses of 10, 20, and 50 ng/kg/min caused significant (p < 0.05) inhibition of the maximum heart rate, heart rate range, and maximum slope of the curve compared to the control baroreflex curve obtained during intracoronary infusion of PGI₂ vehicle. PGI₂ had no significant effect on the minimum heart rate during hypertension. Since PGI₂ is known to stimulate left ventricular receptors, these effects were most likely produced via stimulation of cardiac receptors. In additional experiments using β₁-blockade with metoprolol or cholinergic blockade with atropine methyl bromide, it was shown that PGI₂ attenuates baroreflex-mediated tachycardia by preventing parasympathetic withdrawal completely and by attenuating sympathetic stimulation by approximately 50%. Thus, stimulation of cardiac receptors with intracoronary PGI₂ at doses that had no or little effect on resting arterial pressure and heart rate resulted in potent inhibition of baroreflex tachycardia. These results suggest that PGI₂ may cause attenuation of baroreflex control of heart rate during conditions in which there is an elevation of plasma and/or cardiac PGI₂ levels.