Abstract
A CONJECTURED role of disordered sodium-retaining function of the adrenal cortex in the genesis of essential hypertension has been largely founded on indirect evidence1,2, including the rationale of low-sodium intake3,4 and of naturetic agents5,6 in therapy; and on direct steroid measurements7,8. These latter have shown hyper-excretion of the mineralocorticoid, aldosterone (11β,21-dihydroxy-20-oxo-pregn-4-ene-18-al), arid its major metabolite, tetrahydroaldosterone (3α, 11β,21-trihydroxy-20-oxo-5β-pregnane-18-al), in uncomplicated as well as complicated forms of this disease. These observations have favoured the hypothesis that essential hypertension may represent, in effect, a special form of hyperadrenocorticism. Correlation of normal aldosterone regulation with the renin-angiotensin mechanism in the kidney9,10 has further focused attention on possible regulatory abnormalities of aldosterone in the pathogenesis of arterial hypertension.
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CARR, H., NAUKKARINEN, I. Isolation of a Polar Aldosterone-like Substance from the Urine and Adrenal Incubates of Patients with Arterial Hypertension. Nature 197, 696–697 (1963). https://doi.org/10.1038/197696b0
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DOI: https://doi.org/10.1038/197696b0
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