Sodium and potassium in essential hypertension.

TLDR

The study proposes three hypotheses—cell‑salt, dietary salt, and kidney‑salt—to explain how electrolytes influence arterial pressure in essential hypertension. Researchers measured arterial pressure and electrolyte content in 91 hypertensive patients and 121 normotensive controls. Exchangeable sodium positively correlates with arterial pressure, especially in older patients, while potassium inversely correlates, especially in younger patients, indicating two mechanisms: an early potassium‑driven rise in blood pressure and a later renal lesion that resets pressure natriuresis and increases sensitivity to dietary sodium.

Abstract

A study was carried out of arterial pressure and body content of electrolytes in 91 patients with essential hypertension and 121 normal controls. Exchangeable sodium was found to be positively correlated with arterial pressure in the patients, the correlation being closest in older patients; values of exchangeable sodium were subnormal in young patients; and plasma, exchangeable, and total body potassium correlated inversely with arterial pressure in the patients, the correlations being closest in young patients. Three hypotheses were proposed to explain the mechanisms relating electrolytes and arterial pressure in essential hypertension--namely, a cell-salt hypothesis, a dietary salt hypothesis, and a kidney-salt hypothesis. It was concluded that two mechanisms probably operate in essential hypertension. In the early stages of the disease blood pressure is raised by an abnormal process related more closely to potassium than to sodium. A renal lesion develops later, possibly as a consequence of the hypertension. This lesion is characterised by resetting of pressure natriuresis and is manifest by an abnormal relation between body sodium and arterial pressure and by susceptibility to increased dietary sodium intake.