Renin in the kidneys of rats with aminonucleoside nephrosis

Abstract

An experimental nephrotic syndrome was produced in rats by aminonucleoside administration. Unlike previous results in animals given excess mineralocorticoid, aminonucleoside did not reduce the renin content of the kidney; did not cause an increased sensitivity to single or repeated doses of renin, whether renin was given from the beginning of the experiment or 2 days before edema formation; and did not cause hypertension. The severity of the nephrotic syndrome was augmented by a high-salt diet. The syndrome could be produced in adrenalectomized animals on maintenance doses of desoxycorticosterone acetate, suggesting that the hyperaldosteronism of aminonucleoside nephrosis is not the cause of the observed edema and ascites. Sharp distinctions can be drawn between the mechanisms of edema formation in experimental nephrosis and those of the ‘eclampsia-like’ syndrome.