Ventricular receptors activated following myocardial prostaglandin synthesis initiate reflex hypotension, reduction in heart rate, and redistribution of cardiac output in the dog.

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Abstract
Arachidonic acid (250 micrograms) injected into the left circumflex coronary artery of anesthetized dogs, with carotid arteries tied to reduce baroreflex-induced changes, caused a reduction in heart rate (-15 +/- 1.6 beats/min), mean arterial pressure (-27 +/- 3.4 mm Hg), and left ventricular dP/dt (-939 +/- 138 mm Hg/sec). In contrast, injection of arachidonic acid into the left anterior descending coronary artery caused smaller changes in heart rate (-4.6 +/- 1.6 beats/min), arterial pressure (-14 +/- 2.8 mm Hg), and left ventricular dP/dt (-118 +/- 131 mm Hg/sec). The hypotension following the injection of arachidonic acid results from an increase in perfusion of the kidney and skeletal muscle (as measured by radioactive microspheres), and is entirely reflex, since the changes in renal blood flow, as well as the reduction in heart rate and the hypotension, are eliminated by bilateral vagal section. Increasing the dose of arachidonic acid results in dose-related changes in heart rate, arterial pressure, and left ventricular dP/dt. Prostacyclin and prostaglandin E2, the two principle coronary vasodilator metabolites of arachidonic acid, but not nitroprusside, cause a fall in blood pressure and heart rate, establishing that coronary vasodilation per se is not responsible for initiating the reflex fall in arterial pressure and heart rate. In two dogs with sinoaortic denervation, circumflex injection of arachidonic acid caused larger reductions in heart rate (-21 +/- 1.5 beats/min) and mean arterial pressure (-51 +/- 3.5 mm Hg).(ABSTRACT TRUNCATED AT 250 WORDS)

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