Japanese Heart Journal
Online ISSN : 1348-673X
Print ISSN : 0021-4868
ISSN-L : 0021-4868
Role of the Aldosterone System in the Salt-Sensitivity of Patients with Benign Essential Hypertension
Masao ISHIIKeiichiro ATARASHIToshio IKEDAYasunobu HIRATATomoyuki IGARIYoshio UEHARAMasao TAKAGIHiroaki MATSUOKATadanao TAKEDASatoru MURAO
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1983 年 24 巻 1 号 p. 79-90

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This study compared responses of blood pressure, plasma concentrations of norepinephrine (PNE) and aldosterone (PA), plasma renin activity (PRA) and urinary excretion of aldosterone during a 5-day period of high salt intake in 11 untreated patients with essential hypertension and 11 age-matched normotensive control subjects. The hypertensive patients all had blood pressures that had been above 160 systolic and/or 90mmHg diastolic before admission and had decreased to below 150/90mmHg with only bed-rest and mild salt restriction (6Gm per day). Sodium balance was also measured before and after high salt intake (16Gm per day). The hypertensive patients showed both a significant reduction in blood pressure after hospitalization and a significant blood pressure elevation when salt intake was increased. In contrast, no obvious changes in blood pressure were observed in the normotensive subjects. Sodium retention and decreases in PNE and PRA during the high salt period were similar in both groups. However, the reduction in PA and urinary aldosterone excretion in response to excessive salt intake was less pronounced in the hypertensive patients than in the normotensive subjects. The ratio of percentage changes in PA to percentage changes in PRA after salt loading was significantly lower in the hypertensive patients than in the normotensive subjects. In addition, the changes in PA during salt loading were inversely proportional to changes in blood pressure (r=0.66, p<0.01). Thus, it is suggested that the sensitivity of blood pressure to increased dietary salt intake in hypertensive patients may be related to altered aldosterone dynamics, and that the blunt responses of the PA and urinary excretion of aldosterone can be attributed to reduced sensitivity of the adrenal cortex to changes in circulating angiotensin.
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