α₂-adrenergic stimulation and vasopressin in congestive heart failure

Patients with chronic heart failure (CHF) have increased plasma levels of the antidiuretic hormone arginine vasopressin (AVP). The stimulus for increased AVP secretion is unknown, but appears to involve a non-osmotic drive which alters normal osmoregulatory mechanisms. Centrally acting α₂-adrenergic agonists suppress AVP secretion in experimental animals. To examine the hypothesis that such effects might be apparent on the chronically elevated AVP levels in patients with CHF, we measured AVP, heart rate (HR), mean arterial pressure (MAP), and plasma norepinephrine (NE) after 4 mg oral guanabenz in nine patients with this disease. Plasma NE decreased from 513 ± 131 to a minimum of 371 ± 117 pg/ml (p < 0.02) 5 h postdrug. HR decreased from 80 ± 9.3 to 74 ± 10 beats/min (p < 0.05) and MAP decreased from 88 ± 8.5 to 83 ± 10 mm Hg (p < 0.05). Plasma AVP, however, did not change from baseline levels of 5.6 ± 1.6 pg/ml. Serum osmolality was also constant. These data do not support a possible role for acute increases of α₂-adrenergic activity in suppressing the increased plasma AVP levels of CHF, at least under basal conditions at constant osmolality.