FRANCIS J. HADDY, M.D., Ph.D.
Recent studies suggest that sodium-dependent low-renin hypertension in animals results at least in part from sodium-potassium pump inhibition in blood vessels and heart by a humoral agent released from or influenced by the anteroventral third ventricular area of the brain. For example, a high salt intake in a rat with reduced renal mass results in the appearance of a heat-stable sodium pump inhibitor in the plasma, decreased cardiac Na+, K+-ATPase activity, decreased arterial sodium-potassium pump activity, and hypertension. These changes are reversed by reducing the salt intake or by producing a lesion in the anteroventral third ventricular area of the brain. The course of the development of pump inhibition is similar to the course of the development of hypertension. Sodium-potassium pump inhibition by a humoral agent may also occur in humans with low-renin hypertension. A high potassium intake may stimulate pump activity.
FRANCIS J. HADDY. Sodium-Potassium Pump in Low-Renin Hypertension. Ann Intern Med. 1983;98:781–784. doi: 10.7326/0003-4819-98-5-781
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Published: Ann Intern Med. 1983;98(5_Part_2):781-784.
Cardiology, Coronary Risk Factors, Hypertension, Nephrology.
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