This early basic science study demonstrates that renal extracts inactivate angiotonin through a mechanism distinct from oxidative deamination.
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Hypothesis-generating for renal pressor amine metabolism; leaves open validation in contemporary hypertension models.
(1) Angiotonin is inactivated following incubation with renal extracts. This destruction does not occur by oxidative deaminization since (a) oxygen is not necessary for the reaction, (b) a fraction of kidney extract can be prepared which destroys angiotonin but fails to inactivate hydroxytyramine, and (c) angiotonin is destroyed in the presence of octyl alcohol. (2) Evidence is presented for the existence of an aerobic polyphenolase in kidney extracts, capable of destroying specific pressor amines.
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Bing et al. (1941) studied this question.
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