T. Harioka, Y. Hatano, K. Mori
Mar 1, 1984
Citations
0
Influential Citations
15
Citations
Quality indicators
Journal
Anesthesia & Analgesia
Abstract
In helically cut strips of dog cerebral, mesenteric, and femoral arteries contracted with prostaglandin (PG) F2α, trimethaphan (10-5-10--3 M) caused a dose-related relaxation that was not influenced by atropine, propranolol, diphenhydramine, cimetidine, aminophylline, or indomethacin. Trimethaphan-induced relaxation was greater in extracerebral than in cerebral arteries. The relaxation was greater in phenylephrine-contracted arteries than in PGF2α-contracted arteries. On the other hand, hexamethonium did not relax the arteries. Trimethaphan (10-4-10-3 M) shifted the dose-response curve for norepinephrine in mesenteric arteries to the right, but failed to influence the contractile response to 25 mM KCl. Treatment with trimethaphan (10-4-10-3 M) protected α-adrenergic receptors from persistent blockade by phenoxybenzamine. Trimethaphan (10-7-3 × 10-6 M) and hexamethonium (3 × 10-8-10-6 M) significantly attenuated the contractile response of mesenteric arteries to nicotine in a dose-dependent manner, but did not alter the response to transmural electrical stimulation. The antinicotinic potency of trimethaphan was approximately one-fourth that of hexamethonium. It is concluded that, unlike hexamethonium, trimethaphan acts directly on vascular smooth muscle to induce vasodilation, more prominently in extracerebral arteries than in cerebral arteries. In high concentrations, trimethaphan appears to possess an α-adrenergic blocking action.