The effect of sulfinpyrazone on the response to sympathetic nervous system stimulation.
The purpose of this study was to determine if sulfinpyrazone has a direct action on sympathetic nerve endings to prevent release of the transmitter. Pre-synaptic and post-synaptic events as well as direct sympathetic nervous system stimulation were tested in 15 alpha-chloralose anesthetized cats before and 1 hour after sulfinpyrazone (100 mg . kg-1, i.v.). Heart rate response to cardiac accelerator nerve stimulation or to increasing doses of isoproterenol was not significantly depressed by sulfinpyrazone. In addition, no alteration in the reflex activation of the sympathetic nervous system in response to histamine was observed following sulfinpyrazone. Both norepinephrine and epinephrine levels were similar to those levels reported previously by Smith and Robinson for (7) untreated cats. We conclude sulfinpyrazone has no direct depressing effect on the sympathetic nerve endings and that this mechanism cannot explain the reported beneficial effect of sulfinpyrazone on coronary occlusion induced arrhythmias.
D000818:Animals; D002395:Catecholamines / Q000097:blood; D002415:Cats; D005260:Female; D006339:Heart Rate / Q000187:drug effects; D006632:Histamine / Q000494:pharmacology; D007545:Isoproterenol / Q000494:pharmacology; D008297:Male; D013442:Sulfinpyrazone / Q000494:pharmacology*; D013564:Sympathetic Nervous System / Q000187:drug effects*
D002395:Catecholamines; D006632:Histamine; D007545:Isoproterenol; D013442:Sulfinpyrazone