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5/6th Nephrectomy in Combination with High Salt Diet and Nitric Oxide Synthase Inhibition to Induce Chronic Kidney Disease in the Lewis Rat
Published on: July 3, 2013
The voluntary correction of sodium deficiency by the rabbit
Abstract:
The behaviour involved in the correction of sodium deficit has been studied in wild rabbits and also laboratory bred rabbits. They were offered 0.5 M NaCl to drink. In adrenalectomized wild rabbits variable sodium deficits were produced by withdrawal of mineralocorticoid for 24-72 hr. Correction of the deficit was remarkably precise and was achieved in 9-24 hr, being slower with smaller deficits. That is, the rate of drinking was almost commensurate with the degree of body deficit. No overdrinking occurred by 24 hr. Repetition of the experiment with 24 hr deficiency and with the offer of a cafeteria of 0.5 M NaCl, 0.5 M KCl, 0.25 M CaCl2 and 0.25 M MgCl2 showed the increased appetite was specific for NaCl. Both wild and laboratory rabbits, adrenally intact, were made sodium deficient by the diuretic furosemide. Voluntary salt intake did not peak until 6-12 hr later reflecting the characteristic delay in the genesis of salt appetite. If presentation of salt were delayed 24 hr after furosemide, the highest rate of intake was seen immediately in both wild and laboratory rabbits, but the wild rabbits were much faster in fully correcting body deficit. Infusion of isotonic NaCl, adequate to correct the deficit, given during the third-sixth hour of access to NaCl under the 24 hr delay of presentation regime, halved salt appetite over this period, and by 9-12 hr it was abolished. Polyethylene glycol induced subcutaneous fluid sequestration, salt appetite and thirst but caused an obvious severe deterioration in the animals condition.(ABSTRACT TRUNCATED AT 250 WORDS)

