RENAL SODIUM-EXCRETION AFTER ORAL OR INTRAVENOUS-SODIUM LOADING IN SODIUM-DEPRIVED NORMOTENSIVE AND SPONTANEOUSLY HYPERTENSIVE RATS

Spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (W KY) rats that had been on a low sodium diet for 3 days were given 1.5 mmol sodium chloride kg(-1) body weight either orally or intravenously . The rats receiving an oral sodium load showed a greater natriuresis than those receiving the same saline load intravenously. No increase o f renal sodium excretion was observed when the rats received a hyperto nic mannitol solution orally. The cumulative sodium excretion during t he 8 h following oral loading was two to three times larger in SHR tha n in WKY, whereas no difference between strains could be demonstrated after giving saline intravenously. Furthermore, after switching from n ormal to low sodium diet the rate of decrease of renal sodium excretio n was greater in SHR than in WKY rats. It is proposed that there exist s a gastrointestinal sensory mechanism for sodium controlling the rena l sodium excretion. Furthermore, it is suggested that the function of this mechanism differs between SHR and WKY.