Effects of cholinergic and beta-adrenergic blockade on orthostatic tolerance in healthy subjects

Cardiovascular responses during a graded lower body negative pressure (LBNP ) protocol were compared before and after atropine and propranolol administ ration to test the hypothesis that both sympathetic and parasympathetic con trol of cardioacceleration are associated with syncopal predisposition to o rthostatic stress in healthy subjects. Eleven men were categorized into two groups having high (HT, N = G) or low (LT, N = 5) tolerance based on their total time before the onset of presyncopal symptoms. HT and LT groups were similar in physical characteristics, fitness, and baseline cardiovascular measurements. Atropine treatment had no effect on LBNP tolerance or mean ar terial pressure at presyncope, despite an atropine-induced increase in hear t rate. Propranolol treatment reduced (p < 0.05) LBNP tolerance in both gro ups. Diminished LBNP tolerance after propranolol administration was associa ted with reductions in cardiac output, whereas increase in systemic periphe ral resistance from baseline to presyncope was unaffected by propranolol. R eduction in cardiac output and LBNP tolerance after P blockade reflected a chronotropic effect because lower LBNP tolerance for the HT (-50%) and LT ( -39%) groups was associated with dramatic reductions (p <0.05) in the magni tude of LBNP-induced tachycardia without significant effects on stroke volu me at presyncope. Absence of an atropine-induced difference in cardiac outp ut and systemic peripheral resistance between HT and LT groups failed to su pport the notion that cardiac vagal withdrawal represents a predominant mec hanism that could account for differences in orthostatic tolerance. Because a reduction in LBNP tolerance in both HT and LT groups after propranolol t reatment was most closely associated with reduced tachycardia, the data sug gest that a primary autonomically mediated mechanism for maintenance of mea n arterial pressure and orthostatic tolerance in healthy subjects is beta a drenergic-induced tachycardia.