Time course of adaptation to low and high NaCl diets in the domestic fowl

Abstract

White Plymouth Rock fowls (2.5–5.5 kg, mostly laying hens) were maintained onlow NaCl treatment (L: balanced ration and distilled water; mean Na⁺ intakes 0.2–0.3 m-mole/kg bw.d depending on experiment) orhigh NaCl treatment (H: balanced ration with 1% w/w NaCl+0.5% w/v NaCl drink; mean Na⁺ intakes 10–13.5 m-mole/kg d). DuringNaCl depletion (birds adapted to H, then switched to L for 1, 2, 4 or 8d) plasma aldosterone concentrations rose hyperbolically (half time,t _1/2, 2d) from 2.2±0.3 (SEM;n=7) to 16.9±4.1 (8) pg/100 μl by 8d; prolactin concentrations fell linearly from 25.0±2.3 (10) to 20.5±2.2 (8) ng/ml in the same time. Epithelial short-circuit currents plotted against plasma aldosterone concentrations during NaCl depletion indicate that coprodeum is less sensitive than rectum (colon) to this hormone. Followingresalination (birds adapted to L, then given 10ml 0.75M NaCl/kg orally 24, 16 or 8h before blood sampling), aldosterone concentrations fell from 25.8±1.5 (3) to 3.7±1.6 (3) pg/100 μl and prolactin concentrations rose from 13.8±2.0 (3) to 44.7 ±8.4 (3) ng/ml, both within 8h. Corticosterone concentrations rose briefly following NaCl depletion and resalination, probably due to non-specific “stress”.Electrolyte balance studies (birds adapted to H, then switched to L for 6d, andvice versa (repletion) showed an accumulated change of 12–13m-mole Na⁺/kg, lost during NaCl depletion (t _1/2 0.5d, stabilised by 4–6d) and gained during NaCl repletion (t _1/2 0.5d, stabilised by 2–3d); results were similar for Cl⁻; K⁺ lost during NaCl repletion stabilised by 2d (t _1/2 0.5d) at 5m-mole/kg, but losses continued during depletion at 2.3 m-mole/kg·d through to 6d. It is concluded that the pace of lower intestinal adaptation to dietary Na⁺ levels is probably dictated by the pace of changing Na⁺ balance, via its effect(s) on plasma aldosterone (and possibly prolactin) concentrations, while differences in temporal patterns of adaptation by coprodeum and rectum to NaCl depletion depend on their differential sensitivities to aldosterone. Reciprocating plasma concentrations of aldosterone and prolactin during NaCl depletion-resalination suggest prolactin may be a candidate antagonist to aldosterone actions during states of high NaCl-intake. Changes in K⁺ balance during NaCl depletion-repletion can be explained in terms of linked K⁺−Na⁺ transport by the lower intestine.