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March 14, 1942


JAMA. 1942;118(11):899. doi:10.1001/jama.1942.02830110041015

A study of the amino acid metabolism in the isolated ischemic kidney of laboratory animals has led Bing and Zucker1 of Columbia University to formulate a new theory of the chemical etiology of renal hypertension. Among the numerous metabolic enzymes known to be present in the kidney the Columbia University physiologists emphasize the role of two groups of ferments which transform amino acids into simpler end products. First are a number of specialized catalysts acting directly on amino acids, taking from each its carboxyl group. These decarboxylases thus transform amino acids into corresponding amines. The action of these specialized decarboxylating enzymes is readily demonstrated in aqueous extracts of the renal cortex. The resulting amines may be isolated chemically or titrated by means of their pressor effects on cats. While most amino acids are without appreciable effects on arterial blood pressure, many of the corresponding amines cause arterial hypertension often

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