Life sciences
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Recent evidence suggests that the vascular sodium-potassium pump suppression previously observed in animals with various models of low renin hypertension results from a circulating heat stable ouabain-like agent. It appears to come from or be influenced by the anteroventral third ventricle area of the brain and its action on blood vessels results in depolarization of the smooth muscle cell. Suppression of the vascular sodium-potassium pump, with ouabain for example, increases contractile activity and the contractile responses to vasoactive agents. Thus the humoral pump inhibitor may be involved in the genesis and maintenance of experimental low renin hypertension.