The degree by which atrial natriuretic factor (ANF)-induced renal hemodynamic changes account for its natriuretic effect was determined by early clamp experiments in six anesthetized dogs. After control periods, perfusion pressure of the left kidney (LK) was reduced to 80-90 mmHg, and synthetic ANF (auriculin A) was infused intravenously (0.3 μg · min-1 · kg body wt). After recovery, furosemide (F) was administered as a bolus injection (1 mg/kg body wt). In the right kidney (RK), which served as a time control, ANF increased (P <0.05) glomerular filtration rate (GFR) 16 ± 4% and Na excretion (U(Na)V) 261 ± 63%, whereas it decreased urine osmolality (U(osm)) 36 ± 7% without changing free water clearance. ANF also increased diuresis (V) and kaliuresis (U(K)V). F produced qualitatively the same results without changing GFR. In the clamped LK, ANF failed to increase GFR (22 ± 4 vs. 26 ± 4 ml/min), U(Na)V (30 ± 9 vs. 33 ± 11 μeq/min), V, and U(K)V or to decrease U(osm) (841 ± 97 vs. 840 ± 114 mosmol/kg H2O). F had similar effects in LK as in RK. The data demonstrate that the natriuretic effect of ANF is abolished when its renal hemodynamic actions are impeded. In addition, the results demonstrate that ANF antagonizes renal vasoconstriction in the dog. The results are consistent with the view that the ANF-induced natriuresis is due in great part to an increase in the filtered load of Na into a washed-out inner medulla.
|Title of host publication||American Journal of Physiology - Renal Fluid and Electrolyte Physiology|
|Publication status||Published - 1986|
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