Release of pressor substances from renal grafts originating from rats with renal hypertension.

Abstract

A method is described for grafting kidneys on bilaterally nephrectomized rats without interrupting renal blood flow. Under these conditions, normal kidneys caused a pressor response characterized by a gradual rise in pressure suggesting a continuous endocrine secretion. Kidneys from rats made hypertensive by unilateral clipping of the renal artery, renal encapsulation, or partial infarction were tested during the acute and chronic stages of the experimental disease. Wrapped and infarcted kidneys, as well as the untouched contralateral organs, released little or no pressor substances. On the other hand, clipped kidneys released normal or slightly greater amounts of pressor substances; the eontralateral untouched kidney did not elicit any pressor effect. Morphological examination showed a relationship between presence of nephroselerotic lesions and absence of, or decrease of, reninlike pressor substance released. Both changes are believed to be due to high renal vascular pressure against which the partly clipped kidney is protected. These observations suggest that, if renin is a primary factor in the pathogenesis of renal hypertension, hypertension due to renal artery constriction has a mechanism different from that caused by renal manipulation or infarction.