Role of vasopressin in 24-hour blood pressure regulation in diabetic patients with autonomic neuropathy

To evaluate the role of vasopressin (AVP) on blood pressure (BP) in diabetic patients with autonomic neuropathy (AN), 10 patients were studied on a fixed sodium and potassium diet. On days 4 and 7, a 24-h BP monitoring, as well as blood and urine samples for sodium, potassium, creatinine, and osmolality determinations were obtained for every 4-h period; either placebo or an AVP-V1-antagonist (d(CH2)5Tyr(me)AVP; 0.5 mg; AVPi) were given iv at 1 . On placebo, systolic BP (SBP) showed a progressive elevation during the day, declining after 12 (8 to 12 122 ± 9; 12 to 4 125 ± 11; 4 to 8 134 ± 14; 8 to 12 136 ± 14; 12 to 8 131 ± 17 mm Hg). On AVPi this rise in SBP was blunted: 8 to 12 125 ± 122; 12 to 4 121 ± 21; 4 to 8 126 ± 16; 8 to 12 129 ± 14; 12 to 8 124 ± 12 mm Hg. Creatinine clearance and diureses were greater during the night, both with placebo and AVPi. Plasma osmolality did not change on either day, although serum sodium decreased after AVPi, reaching the lowest values at 4 to 8 period (137 ± 4.7 v 131 ± 3.8 mEq/L; P< .05). With placebo, fractional excretion of sodium (FENa) increased from 0.43% ± 0.32% during 12 h of orthostasis to 0.92% ± 1.05% during 12 h of recumbency (P< .02). With AVPi, the FENa on orthostasis did not differ from that with placebo, although BP values were lower and did not increase with recumbency (0.58 ± 0.57 v 0.73% ± 0.49%; NS). In conclusion, our results show that in diabetic patients with AN, vasopressin participates in BP control by stimulating vascular and renal V1 receptors, which results in vasoconstriction and sodium reabsorption.