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

Autor: Hintze, Thomas H., Kaley, Gabor, Panzenbeck, Maret J.
Zdroj: British Journal of Pharmacology; May 1984, Vol. 82 Issue: 1 p117-125, 9p
Abstrakt: 1In the cat, intravenous injections of arachidonic acid or prostaglandin (PG)F2αcaused 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.2In cats with bilateral ligation of the carotid arteries to eliminate competition between systemic baroreflexes and cardiopulmonary reflexes, PGI2, PGF2αand arachidonic acid caused significantly greater hypotension and bradycardia than in cats with intact carotid baroreflexes.3The bradycardia to PGI2, PGF2αand arachidonic acid was eliminated by bilateral vagal section or atropine.4PGE1, PGE2and nitroprusside caused dose‐related falls in mean arterial pressure and a small tachycardia.5In a small group of cats (7 of 67) nitroprusside also caused a reduction in heart rate which was eliminated by indomethacin.6We conclude that the reflex bradycardia to PGF2α, like that to arachidonic acid is, at least in part, the result of the stimulation of synthesis of another prostaglandin, most likely PGI2. In the cat, intravenous injections of arachidonic acid or prostaglandin (PG)F2αcaused 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, PGF2αand arachidonic acid caused significantly greater hypotension and bradycardia than in cats with intact carotid baroreflexes. The bradycardia to PGI2, PGF2αand arachidonic acid was eliminated by bilateral vagal section or atropine. PGE1, PGE2and 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 PGF2α, like that to arachidonic acid is, at least in part, the result of the stimulation of synthesis of another prostaglandin, most likely PGI2.
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