Vascular effects alter early-gestation fetal renal responses to vasopressin.

Abstract

Distinct receptors mediate the vascular (V1) and renal (V2) effects of arginine vasopressin (AVP). Although ovine fetal AVP-induced antidiuresis can be demonstrated in early gestation (< 120 days; term 150 days), the early-gestation fetal renal responses to AVP are variable, including increases in urine flow and glomerular filtration rate (GFR). AVP V1 receptor predominance and/or V2 receptor system immaturity may contribute to variable early-gestation renal responses to AVP. To differentiate these possibilities, we assessed early-gestation fetal V2 receptor function in the presence and absence of V1 receptor-mediated effects by comparing the responses to AVP (a combined V1-V2 receptor agonist; n = 10; 112 +/- 2 days) with the selective V2-receptor agonist 1-desamino-8-D-arginine vasopressin (DDAVP) (n = 5; 111 +/- 2 days). AVP infusion increased fetal mean arterial pressure (MAP; 36 +/- 1 to 44 +/- 2 mmHg) and decreased heart rate (197 +/- 2 to 171 +/- 3 beats/min); DDAVP infusion had no effect on MAP or heart rate. Free water clearance decreased in response to AVP (0.13 +/- 0.02 to 0.02 +/- 0.01 ml.min-1.kg-1) and DDAVP (0.21 +/- 0.04 to 0.04 +/- 0.02 ml.min-1.kg-1), and urine osmolality increased in response to both analogues (AVP: 145 +/- 4 to 283 +/- 15 mosmol/kgH2O; DDAVP: 146 +/- 5 to 244 +/- 32 mosmol/kgH2O).(ABSTRACT TRUNCATED AT 250 WORDS)