Abstract
In fasting normotensive subjects, auscultatory blood pressures and pulse responses to histamine base (.025 mg intravenously), Mecholyl (10 mg subcutaneously), tetraethylammonium chloride (TEAC 400 mg intravenously) and atropine sulfate (1.2 mg intravenously) were recorded during control periods and during constant infusion of 1-epi-nephrine (.085 [mu]g/kg/minute) and l-norepinephrine (.085 [mu]g /kg/minute). Both TEAC and atropine dramatically potentiated the pressor response to norepinephrine (TEAC, +33/20 mm Hg; atropine, +45/35 mm Hg) but did not potentiate epinephrine. Mecholyl and histamine were consistently depressor during epinephrine and norepinephrine infusions. Cardiac outputs measured before and during potentiation of nor-epi-nephrine by TEAC or atropine revealed a significant increase (atropine, 2.4 l/minute; TEAC, 1.38 l/minute). In pheochromocytoma a positive provocative test with TEAC represents a potentiation phenomenon specific for circulating norepinephrine. Atropine, like TEAC, potentiates norepinephrine and should be evaluated as a screening agent for pheochromocytoma. Pressor potentiation of norepinephrine by TEAC or atropine is likely due to blockade of carotid sinus and aortic arch reflexes controlling cardiac rate and is not due to changes in peripheral resistance.