Human urinary natriuretic factor exhibits smooth muscle contractile properties that correlate with its natriuretic activity and, relative to kallikrein excretion, with patient blood pressure.
Hypothesis-generating for natriuretic factor's vasoactive role; leaves open human translation and clinical relevance.
Human urine contains a small molecular weight natriuretic substance and similar material isolated from the kidney inhibits Na/K ATPase. Such action on smooth muscle in blood vessels would cause contraction. Human urinary natriuretic material caused contraction of the smooth muscle in the rat anococcygeus muscle and this activity correlated with its natriuretic activity. Known vasoactive substances could not explain the activity of the natriuretic factor when tested on the anococcygeus muscle. The best correlation with blood pressure of the patient was with the log of the ratio of natriuretic activity divided by the kallikrein excretion. A normotensive woman with severe renal failure had very high kallikrein excretion as well as increased natriuretic activity and her data fitted the same correlation as the hypertensives' data.
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Mills et al. (1985) studied this question.
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