Mechanisms of reflex bradycardia and hypotension by metabolites of arachidonic acid in the cat.

摘要

In the cat, intravenous injections of arachidonic acid or prostaglandin (PG)F2 alpha caused significant reductions in mean arterial pressure and heart rate which were eliminated or significantly lessened, respectively, by previous administration of indomethacin. The bradycardia to intravenous prostacyclin (PGI2) was unaffected by indomethacin. In cats with bilateral ligation of the carotid arteries to eliminate competition between systemic baroreflexes and cardiopulmonary reflexes, PGI2, PGF2 alpha and arachidonic acid caused significantly greater hypotension and bradycardia than in cats with intact carotid baroreflexes. The bradycardia to PGI2, PGF2 alpha and arachidonic acid was eliminated by bilateral vagal section or atropine. PGE1, PGE2 and nitroprusside caused dose-related falls in mean arterial pressure and a small tachycardia. In a small group of cats (7 of 67) nitroprusside also caused a reduction in heart rate which was eliminated by indomethacin. We conclude that the reflex bradycardia to PGF2 alpha, like that to arachidonic acid is, at least in part, the result of the stimulation of synthesis of another prostaglandin, most likely PGI2.