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1 Departments of Pharmacology and Hygiene, Faculty of Medicine, Kyoto University, Kyoto, Japan
In anesthetized dogs i.v. injections of capsaicin (10-300 µg/kg) caused a transient rise in mean systemic blood pressure followed by a sustained fall, whereas in anesthetized rabbits capsaicin caused only hypotension. The induced hypertension in dogs was not influenced by treatment with hexamethonium, tolazoline and phentolamine. The hypo tension in dogs and rabbits was diminished by atropine. In atropine-treated dogs the heart rate was not influenced or was increased slightly by capsaicin in spite of a marked rise in blood pressure. Capsaicin (2 x 10-8 to 2 x 10-6 g/ml) did not influence the rate or the contractile force of isolated dog and rabbit atria. Capsaicin caused a sustained in crease in the tension of spiral strips of proximal and distal mesenteric arteries and proxi mal and distal renal arteries of the dog. The tension increment was not significantly altered by phentolamine. The contractile effect of capsaicin in dog superior mesenteric arteries was slightly reduced by decreasing [Ca++]o to 0.73 mM (1/3 normal [Ca++]o) and was abolished by removal of Ca++ from the bathing media. Strips of dog coronary artery showed contracture in response to capsaicin but showed relaxation in response to nor epinephrine. Cerebral arterial strips also contracted after capsaicin administration. On the other hand, strips of dog aorta and main pulmonary artery did not respond to capsaicin. Capsaicin did not increase the tension of strips of rabbit aorta, main pulmo nary artery and superior mesenteric artery. The contractile response of rabbit ascending aorta to transmural electrical stimulation at 5 and 20/sec was potentiated and prolonged by 2 X 10-6 and 10-5 g/ml capsaicin. These findings suggest (1) that the depressor re sponse of dogs and rabbits to capsaicin is associated with cholinergic mechanisms, (2) that capsaicin causes hypertension in dogs by its action on peripheral vasculatures but not on the heart and (3) that capsaicin-induced vasoconstriction is related intimately to extracellular Ca++ but not to an adrenergic mechanism.
Submitted on October 4, 1971
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