Cardiovascular counterregulation during sympathetic inhibition in normal subjects and patients with mild hypertension.

Abstract

The influence of agents that inhibit sympathetic nerve activity on cardiovascular responsiveness, as related to major pressor factors, has been unclear. Therefore, these components were evaluated in 11 normal subjects and 13 patients with mild essential hypertension, before and after 4 wk of sympathetic neuron blockade with the agent debrisoquine. In these normal and mildly hypertensive subjects, sympathetic neuron blockade caused approximately similar decreases in urinary and supine or upright plasma norepinephrine (NE) levels (average changes in the 2 groups, -41% and -45%, respectively; P < 0.05 to < 0.005), the chronotropic dose of isoproterenol (-45% and -38%), and the NE pressor dose (-47% and -51%, P < 0.01), while the relationship between NE-induced changes in blood pressure and concomitant plasma NE concentrations was displaced to the left (P < 0.01). Supine heart rate was also lowered (-10% and -8%, P < 0.05). Compared to the orthostatic variations during placebo conditions, mild postural decreases in blood pressure were apparent in both normal and hypertensive groups (-8% and -7.5%). However, supine blood pressure was unchanged following debrisoquine treatment. Other parameters were also not consistently changed, such as: total blood volume, exchangeable body Na, urinary electrolytes, plasma epinephrine, renin and angiotensin II (AII) levels, the pressor dose of infused AII, and the relationship between AII-induced changes in blood pressure and plasma AII measured before and during AII infusion. The reduction in sympathetic outflow during sympathetic neuron blockade may elicit a hyperresponsiveness of .alpha.- and .beta.-adrenergic receptors that is equal in normal subjects and patients with mild essential hypertension.