ARGININE-VASOPRESSIN INTERACTS WITH THROMBOXANE IN HYDRONEPHROSIS

The influence of hydronephrosis (6-10 wk) on the renal vascular respon se to arginine vasopressin (AVP) was assessed, using isolated perfused normal and hydronephrotic rat kidneys. In normal kidneys, AVP (0.3 nM ) reduced renal perfusate flow (RPF) by 55 +/- 7% (P < 0.01). AVP-indu ced decrements in RPF were reversed partially by diltiazem (10 l-IM) a nd completely by 10 nM of an AVP (V-1)-receptor antagonist (AVPX). In hydronephrotic kidneys, AVP reduced RPF by 81 +/- 2% (P < 0.01) and co nstricted afferent (AA) and efferent arterioles (EA) by 33 +/- 3 (P < 0.01) and 33 +/- 5% (P < 0.01), respectively. The addition of diltiaze m altered neither RPF nor vessel diameters. Administration of AVPX rec overed RPF, AA, and EA diameters. When hydronephrotic kidneys were pre treated with thromboxane (Tx) inhibitors, AVP reduced RPF by 62 +/- 5% (P < 0.01) and constricted AAs and EAs by 26 +/- 2 (P < 0.01) and 17 +/- 3% (P < 0.05), respectively. Under Tx blockade, diltiazem partiall y reversed the AVP-induced reduction in RPF and restored the decrement s in AA diameter. Subsequent addition of AVPX returned RPF and EA diam eter. Our data indicate that AVP elicits substantial renal microvascul ar constriction and suggest that AVP stimulates Tx production in hydro nephrotic kidneys, thereby altering renal vascular responsiveness to t his peptide.