vasopressin--1-(1-mercaptocyclohexaneacetic-acid)-2-(o--methyl-l-tyrosine)-8-l-arginine- and Bradycardia

The cardiovascular effects of centrally administered cholinomimetics were examined in conscious Long-Evans and Brattleboro rats. Carbachol (1 microgram/kg) or physostigmine (50 micrograms/kg) induced a long-lasting increase in blood pressure and a decrease in heart rate in Long-Evans rats whereas no bradycardia was observed in Brattleboro rats, and the pressor response was significantly less than that in Long-Evans rats. The cardiovascular responses to nicotine (30 micrograms/kg) in Brattleboro rats were not different from those in Long-Evans rats. Intravenous vasopressin antagonist, d(CH2)5Tyr(Me) arginine vasopressin, significantly attenuated the pressor response and eliminated the bradycardic response to carbachol in Long-Evans rats. However, the pressor response to carbachol in Brattleboro rats was still significantly less than that in Long-Evans rats treated with vasopressin antagonist. Intravenous phentolamine partially inhibited the pressor response to carbachol in Long-Evans rats and completely eliminated it in Brattleboro rats. Combined intravenous treatment with phentolamine and vasopressin antagonist completely eliminated the pressor response to carbachol in Long-Evans rats. Centrally administered methylatropine eliminated either the hypertensive or bradycardic response to carbachol in Long-Evans rats. These results indicate that the pressor and bradycardic response to carbachol or physostigmine is mediated by the central muscarinic receptor mechanism. Hypertensive response to intracerebroventricularly administered carbachol in normal rats is mediated both by an increase in central sympathetic outflow and in circulating vasopressin. The bradycardia seems to be mediated mainly by vasopressin.

Topics: Animals; Arginine Vasopressin; Atropine Derivatives; Autonomic Nervous System; Blood Pressure; Bradycardia; Carbachol; Cardiovascular Physiological Phenomena; Cardiovascular System; Deamino Arginine Vasopressin; Hypertension; Injections, Intraventricular; Male; Nicotine; Parasympatholytics; Phentolamine; Physostigmine; Rats; Rats, Brattleboro; Vasopressins

Other investigators have reported that intravenous infusion of synthetic arginine vasopressin into fetal lambs increases mean arterial pressure and decreases heart rate. To determine if the bradycardia produced by arginine vasopressin is a reflex response to the increase in blood pressure, we studied the effect of arginine vasopressin infusion on heart rate with and without blocking the increase in blood pressure. We performed 34 experiments in 12 chronically cannulated fetal lambs between 103 and 137 days' gestation. All animals had normal blood gas and pH values. Infusion of arginine vasopressin increased mean arterial pressure 10.1 +/- 1.1 mm Hg and decreased heart rate 50 +/- 8 bpm. Fetal heart rate decreased similarly when arginine vasopressin was infused and the hypertensive response was blocked with nitroprusside or a selective vasoconstrictor antagonist. [1-(beta-mercapto-beta,beta-cyclopentamethylene propionic acid) 2-(O-methyl)tyrosine] arginine vasopressin. For comparison we also studied five adult nonpregnant ewes. Bradycardia was observed in the adults after infusion of arginine vasopressin alone and when the hypertensive response was blocked with the vasoconstrictor antagonist. We conclude that arginine vasopressin infusion causes a fall in heart rate independent of any increase in blood pressure in both the fetal lamb and the adult sheep.

Topics: Animals; Arginine Vasopressin; Blood Pressure; Bradycardia; Female; Fetus; Heart Rate; Heart Rate, Fetal; Nitroprusside; Pregnancy; Sheep