HEAT LABILITY OF A DEPRESSOR SUBSTANCE PRESENT IN HUMAN URINE: EFFECTS OF SECTION OF VAGUS NERVES, LIGATION OF CAROTID ARTERY AND OF AUTONOMIC BLOCKADE UPON DEPRESSOR RESPONSE

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Abstract
The depressor effect of urine was studied by recording thedecrease in mean arterial pressure (-MAP) produced by intraven. injn. of the urine into anesthetized dogs. Analysis of results suggests that the mean of the response to a set of 3 injns. must differ by [plus or minus] 50% from that of another set to be significant, and that the apparent concn. of a dilator substance estimated by this method may differ from the true concn. by -50% to + 100%. Evidence is presented that, in addition to callicrein, there is present in normal dialyzed human urine a substance which causes a decrease in the mean arterial pressure of dogs anesthetized with amytal Na when the urine sample is injd. intraven. This depressor substance is somewhat heat labile at 100[degree]C, but it is not completely destroyed by refluxing the urine sample for 1 hr. The urine sample may be concd. by vacuum distillation at 38[degree] to 40[degree]C, and the depressor substance is recovered almost quantitatively in the residue from the distillation. The apparent activity of the depressor substance is increased by bilateral vagal section; it is decreased by subsequent bilateral carotid artery ligation. Intraven. injn. of 200 mg. of tetra-ethyl ammonium chloride (Etamon) and injn. of 10 mg. of benzazoline hydrochloride, 2 benzylimidazoline hydrochloride (Priscol) increase the depressor response to the urine. The possible relationship of this substance to hypertension is discussed.

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