Effects of angiotensin II on plasma antidiuretic hormone and renal water excretion

Effects of angiotensin II on plasma antidiuretic hormone and renal water excretion. The effects of intravenous (i.v.) and intracarotid (IC) angiotensin II (AII) infusion on systemic and renal hemodynamics, renal water excretion, and plasma antidiuretic hormone (ADH) levels were examined in six conscious dogs under water loaded and hydropenic conditions. In the first group of seven studies, AII in a mean dose of 12.7 ng/kg/min was administered i.v. to water loaded dogs. The infusion induced a significant increase in mean arterial pressure (MAP, 99 to 118mm Hg, P < 0.001), and significant reductions in both glomerular filtration rate (GFR, 67 to 57 ml/min, P < 0.05) and para-aminohippurate clearance (CPAH, 280 to 212 ml/min, P < 0.005) occurred. Despite this decrement in renal hemodynamics, urine remained maximally dilute (Uosm, 58 to 61 mOsm/kg H2O, NS). Furthermore, plasma ADH was suppressed maximally after water load and did not increase after i.v. AII infusion. The IC infusion of AII (mean dose 5.8 ng/kg/min) produced similar changes in hemodynamics; plasma ADH remained undetectable. When AII was administered i.v. to hydropenic animals (mean dose 8.3 ng/kg/min), MAP again increased (86 to 111mm Hg, P < 0.001) as GFR (81.3 to 68.6 ml/min, NS) and CPAH (291 to 223 ml/min, P < 0.05) declined modestly. In these animals, Uosm decreased significantly (1429 to 1114 mOsm/kg H20, P < 0.005) and plasma ADH did not change significantly (1.66 to 1.88 pg/ml, NS). When IC AII (4 ng/kg/min) was repeated in hydropenic dogs pretreated with indomethacin, neither Usom (1787 to 1664 mOsm/kg H2O, NS) nor plasma ADH were altered. In summary, these results provide no evidence for an effect of AII to alter water excretion or plasma ADH either in the presence or absence of prostaglandin inhibition