Role of increased glomerular filtration rate in atrial natriuretic factor-induced natriuresis in the rat

Abstract

One of the major renal hemodynamic actions of atrial natriuretic factor (ANF) is to increase glomerular filtration rate (GFR). To assess the role of this effect on ANF-induced natriuresis (U NaV), diuresis (V) and kaliuresis (U KV) we performed late clamp experiments in six rats. After control periods (C), synthetic ANF (auriculin A) was infused i.v. (2μg.min −1/kg body wt) throughout the experiment (150 min). After pre-clamp periods, the perfusion pressure of the left kidney (LK) was reduced to 75–80 mmHg. The right kidney (RK) served as a time control. In LK, before the late clamp, ANF increased (p < 0.01) GFR from 1.5±0.1 to 1.8±0.1 ml/min, V from 17±5 to 53±5 μl/min, and U NaV from 2.1±0.6 to 10.0±0.9 μEq/min. Almost identical increases occurred in the RK. The late clamp returned all parameters in LK to C values (p > 0.05): GFR to 1.4±0.1 ml/min, V to 6.3±1.2 μl/min, and U NaV to 0±0.3 μEq/min. The late clamp also reversed the ANF-induced increase in U KV. In the RK, GFR (1.8±0.1 ml/min), V (38±4 μl/min) and U NaV (7.8±0.8 μEq/min) remained elevated (p < 0.01 vs. C) to the end of the experiment. These data demonstrate that upon return of GFR to control levels, the ANF-induced diuresis, natriuresis and kaliuresis is abolished. The results support our previous view that the increase in GFR together with a decrease in inner-medullary hypertonicity account wholly or in great part for the natriuretic action of ANF.