Sodium-potassium pump in low-renin hypertension.
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.
D000818:Animals; D004032:Diet; D006801:Humans; D006973:Hypertension / Q000188:drug therapy / Q000209:etiology / Q000378:metabolism* / Q000503:physiopathology; D006977:Hypertension, Renal / Q000378:metabolism*; D007473:Ion Channels / Q000378:metabolism*; D009318:Natriuresis; D045283:Natriuretic Agents; D011188:Potassium / Q000378:metabolism* / Q000627:therapeutic use; D011506:Proteins / Q000502:physiology; D051381:Rats; D012964:Sodium / Q000378:metabolism*; D012965:Sodium Chloride / Q000009:adverse effects
D007473:Ion Channels; D045283:Natriuretic Agents; D011506:Proteins; D012965:Sodium Chloride; D012964:Sodium; D011188:Potassium