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The properties of anephrotensin, a polypeptide liberated by acid incubation of serum, are reviewed. Experiments with antirenin rule out the possibility that renin is the enzyme that liberates anephrotensin. Serum anephrotensinogen increases after bilateral nephrectomy or after several weeks of treatment with desoxycorticosterone (DCA). There are perallel changes under these conditions in the amounts of anephrotensinogen and angiotensinogen in the serum, suggesting that a common substrate may be involved. The increase in substrate is in accord with the possibility that DCA treatment results in some deficiency in the handling of proteins by the kidney. There is an increase in urine vasoactive peptides and total proteins in DCA-treated rats. These increases are probably related to deficiency in tubular reabsorption. The increase in the albumin/globulin ratio of the urine proteins under these circumstances supports this idea. The changes described above are not necessarily related to the onset of hypertension. Whether the changes in protein handling by the kidney are related to the hypertension produced by DCA treatment is an unsettled question.

Vasoactive Peptides and Substrates and Their Relation to Protein Handling by the Kidney