SALT METABOLISM IN HYPERTENSION

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Abstract
NaCl metabolism in essential hypertension is abnormal. Patients with essential hypertension may have a slightly elevated serum Na concentration, expanded total body Na content, and increased amounts of Na and water in their arterial wall. Hypertension may be alleviated by Na depletion. Chlorothiazide, a potent natruretic agent, may exert an antihypertensive animals and patients. This drug potentiates the effect of various antihypertensive regimens. The concomitant administration of chlorothiazide reduces the requirement for ganglionic blocking drugs in the treatment of hypertension. Sympathectomized patients are unusually responsive to the blood pressure lowering effect of chlorothiazide. The increased renal tubular rejection of Na, Cl and water in response to salt loading, which is present in essential hypertension, is felt to be the result of the elevated blood pressure and not its cause. There is no evidence that water excretion, occurring in excess of Na excretion, causes a "relative retention" of Na in the majority of hypertensive patients. The hypothesis is discussed that in essential hypertension the Na content of certain compartments or tissues, possibly vascular smooth muscle, may be increased and lead to the elevation of the blood pressure. The effectiveness of chlorothiazide in the treatment of some cases of hypertension might be through its ability to deplete these tissues of Na; in other instances it appears to act through depletion of the plasma volume.

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