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Lead administered to semi-fasted rats caused an elevation of urinary sodium excretion but no increase of urinary potassium excretion as previously observed in fasted rats. Moreover, in this experiment it was found that urinary and serum prostaglandin E2 (PG E2) contents were increased in association with the elevation of urinary sodium excretion by lead and that natriuresis was suppressed by indomethacine treatment. These findings suggest a stimulation of prostaglandin synthetase rather than to a suppression of the renin-angiotensin-aldosterone system as a primary reaction caused by the lead administration.
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