BARORECEPTOR-MEDIATED RELEASE OF VASOPRESSIN IN PATIENTS WITH CHRONIC CONGESTIVE-HEART-FAILURE AND DEFECTIVE SYMPATHETIC RESPONSIVENESS

In patients with congestive heart failure (CHF), overactivity of the sympathetic nervous system may be accompanied by an impairment of the baroreflex control mechanism. To evaluate the reflex responses of the sympathetic nervous system, the renin-angiotensin system and vasopressin release to baroreceptor unloading, 38 patients with left ventricular dysfunction were studied. Hemodynamic data, and plasma norepinephrine, renin activity and vasopressin concentrations were measured before and 60 minutes after administration of high-dose hydralazine (0.4 mg/kg intravenously). On the basis of blood pressure response to vasodilator administration, patients were divided arbitrarily into those with a decrease in mean arterial blood pressure greater-than-or-equal-to 15 mm Hg (group A; n = 12) and those with a decrease <15 mm Hg (group B; n = 26) compared with control values. In response to hydralazine, heart rate decreased in group A from 100 to 92 beats/min (p <0.001) and increased in group B from 90 to 96 beats/min (p <0.05). In group A, hemodynamic changes induced by hydralazine were accompanied by a decrease in plasma norepinephrine from 822 to 518 pg/ml (p <0.01) and an increase in plasma vasopressin from 8.4 to 45.2 pg/ml (p <0.001). In group B, plasma norepinephrine and vasopressin did not change significantly (407 vs 447, and 8.4 vs 8.3 pg/ml, respectively). Plasma renin activity remained unchanged in group A and increased in group B (p <0.001). The data show that baroreceptor-mediated release of vasopressin is not impaired in patients with CHF and a defective sympathetic reflex control mechanism. Thus, baroreceptor-mediated vasopressin release may represent a protective mechanism to maintain systemic blood pressure in a subgroup of patients with severe CHF.