Role of angiotensin AT1 receptor in the cardiovascular response to footshock

Abstract

This study assessed the effect of non-peptide angiotensin II receptor subtype antagonists on the cardiovascular response to footshock. Effects of electric stimulation (1, 2 or 5 Hz) on mean arterial pressure (MAP) and heart rate (HR) were determined. Peripheral or central administration of losartan, an angiotensin AT1 receptor antagonist (1 or 10 mg/kg s.c., or at 10, 30 or 100 micrograms/5 microliters i.c.v.), inhibited the mean arterial pressure response but not the heart rate response to footshock. In contrast, the MAP response to exogenous administration of norepinephrine was not inhibited by subcutaneous administration of losartan (10 mg/kg). Given at 100 micrograms/5 microliters i.c.v., the angiotensin AT2-selective receptor antagonist, PD 123319, did not reduce hemodynamic responses to electric stimulation. These results suggest that, in acute stress, endogenous angiotensin II facilitation of noradrenergic transmission is mediated through the angiotensin AT1 receptor.