STUDIES ON THE MECHANISM OF EXPERIMENTAL PROTEINURIA

Abstract

When renin is administered intramuscularly to the rat, massive proteinuria occurs without a significant elevation of mean arterial blood pressure. The intravenous administration of renin to normal rats results in a great increase in urinary protein excretion. This response to renin is abolished by bilateral adrenalectomy. While the adrenalectomized rat fails to respond to intravenous renin with increased proteinuria, it does exhibit a normal elevation in mean arterial blood pressure. It is concluded that in the rat, the proteinuric property of renin is not related to the ability of this compound to elevate arterial blood pressure. The passage of plasma proteins has been followed through the kidney and into the urine by attaching them to the dye T-1824 (Evan's blue). The intra-peritoneal injection of renin causes a massive, transient proteinuria in the rat. From a study of frozen sections of the kidney of rats whose plasma proteins are labelled with T-1824, it is concluded that the preponderant basis for renin proteinuria is an increase in glomerular permeability.