Plasma aldosterone in essential hypertension.
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Essential hypertension
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We examined corticosteroid secretory patterns and their relation to altered salt and water metabolism in Milan hypertensive and normotensive rats. Hypertensive rats had significantly higher blood pressures, exchangeable sodium (hypertensive, 41.2 +/- 0.3 mmol.kg-1; normotensive, 38.4 +/- 0.03 mmol.kg-1, P < .001), plasma volume (hypertensive, 5.39 +/- 0.12 mL.100 g-1; normotensive, 4.84 +/- 0.10 mL.100 g-1, P < .001), and plasma concentrations of atrial natriuretic peptide (hypertensive, 38.8 +/- 4.0 pg.mL-1, normotensive, 22.4 +/- 3.1 pg.mL-1, P < .02). These features coincide with those of mineralocorticoid-induced hypertension. Adrenal venous secretory rates (picomoles per minute) of corticosterone (hypertensive, 1696 +/- 202; normotensive, 873 +/- 139), 18-hydroxycorticosterone (hypertensive, 49.7 +/- 8.3; normotensive, 25.7 +/- 3.3), and aldosterone (hypertensive, 1.16 +/- 0.17; normotensive, 0.52 +/- 0.08) were higher in the hypertensive than the normotensive strain, but that of 11-deoxycorticosterone (DOC) (hypertensive, 94.4 +/- 14.9; normotensive, 114.3 +/- 33.9) was similar in the two strains. The corticosterone-DOC, 18-hydroxycorticosterone-DOC, and aldosterone-DOC ratios were higher in the hypertensive than the normotensive strain (P < .02), but the 18-hydroxycorticosterone-corticosterone and aldosterone-18-hydroxycorticosterone ratios were not. These results indicate increased activity of the "late" aldosterone biosynthetic pathway in the hypertensive compared with the normotensive strain caused by an increased conversion rate of DOC to corticosterone. The comparison of corticosterone secretion between the two strains indicates that 11 beta-hydroxylase rather than aldosterone synthase activity is more active in the hypertensive than the normotensive rats.
Corticosterone
Mineralocorticoid
Essential hypertension
Hyperaldosteronism
Aldosterone synthase
Primary Aldosteronism
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The response of plasma aldosterone (PA) and plasma renin activity (PRA) to ACTH stimulation (0.25 mg Tetracosactide infusion/10 h) and to insulin-induced hypoglycemia (0.1 U/kg b.w.) has been studied in 34 essential hypertensive (EH) patients. Corticotrophin stimulation increases significantly PA, the percent increase being higher in normal PRA EH patients than in controls but comparable to controls in low PRA EH patients. PRA shows a slight and transient elevation. A significant increase in PA is observed also during the insulin test, but the percent increase is lower than that under ACTH stimulation. The possibility that aldosterone is involved, under severe and frequent stress, in the genesis of essential hypertension is discussed.
Plasma renin activity
Essential hypertension
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The relationship between plasma atrial natriuretic peptide (ANP), renin-angiotensin-aldosterone system and left ventricular mass in essential hypertension was assessed.Immunoreactive ANP in 10 normal subjects and 20 untreated patients with mild to moderate essential hypertension was compared with echocardiographic measurement of cardiac size, function and blood pressure. Venous plasma concentrations of ANP were also studied in relation to urinary sodium and potassium excretion, as well as the renin-angiotensin-aldosterone system.Plasma ANP was higher in hypertensive patients (25.3 +/- 13.3 pg/ml; p = 0.003) than normotensive subjects (11.1 +/- 2.7 pg/ml). In hypertensive patients, plasma ANP was inversely related to plasma renin activity (PRA) (r = -0.6; p = 0.009). No relationship was found between ANP and blood pressure, nor between the indices of left ventricular mass and function or urinary electrolytes.This study showed that circulating ANP is, in average, significantly increased in hypertensive patients, consistent with previous reports. Our data do not support a direct link between left ventricular mass and increased plasma ANP levels in hypertensive patients. Whether the inverse relationship between ANP and PRA in this pathologic state is a direct one or merely a secondary association has not been clearly established.
Atrial natriuretic peptide
Plasma renin activity
Essential hypertension
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Plasma concentrations of progesterone (P), deoxycorticosterone (DOC), 17-hydroxyprogesterone (17-OH P), corticosterone (B), deoxycortisol (S), cortisol (F), and aldosterone were measured in 8 control subjects and in 10 patients with low and normal renin essential hypertension (EH) before and 4 and 8 h after an iv infusion of 25 units of ACTH. Secretion rates of 18-hydroxy-11-deoxycorticosterone (18-OH DOC) were measured for the 24 h prior to and the day of the ACTH infusions. The hypertensive patients had significantly higher plasma levels of aldosterone, DOC and S after ACTH than the controls, whereas plasma B levels were significantly lower. The low renin subgroup considered separately had significantly higher plasma levels of aldosterone and DOC than controls, and higher levels of B and lower levels of F than the normal renin subgroup in response to ACTH. Although not significantly different, the plasma levels of P and the secretion rate of 18-OH DOC tended to be higher, and plasma 17-OH P and F levels lower after ACTH in patients with EH than in controls. The low renin subgroup tended to have the highest plasma S levels and 18-OH DOC secretory rates and lowest F levels. Estimations of adrenal 11beta-hydroxylating efficiency in response to ACTH in patients and controls by plasma steroid ratios revealed significantly lower B/DOC ratios in both low and normal renin patients compared to controls, supported by somewhat lower F/S ratios in these patients, especially those in the low renin subgroup. Altered 17-hydroxylating efficiency seen by significantly lower 17-OH P/P ratios were also found in those with EH, supported by somewhat lower F/B and S/DOC ratios in these patients, agian especially in the low renin subgroup. These data are compatible with a pattern of altered adrenocortical steroid biosynthesis in essential hypertension bearing features similar to adrenal 11beta and 17alpha-hydroxylation deficiencies.
Plasma renin activity
Corticosterone
Essential hypertension
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Plasma levels of atrial natriuretic peptide (ANP) were measured in outpatients with borderline hypertension (n = 15) and essential hypertension (n = 13) and in normotensive subject (n = 11). There were no significant differences among the three groups in age, serum protein, albumin, or electrolyte levels, plasma renin activity (PRA), or plasma concentrations of aldosterone and cortisol. The plasma ANP levels in the normotensive, borderline hypertensive, and essential hypertensive subjects were 36 +/- 6 pg/ml (mean +/- S.E.), 64 +/- 11 pg/ml, and 82 +/- 14 pg/ml, respectively. The levels in the essential hypertensive subjects were significantly (p less than 0.05) higher than those in the normotensives. In both borderline and essential hypertensives (n = 28), the plasma ANP levels were significantly correlated positively with systolic blood pressure (r = +0.385, p less than 0.05), and negatively with PRA (r = -0.484, p less than 0.05) and serum total calcium (r = -0.516, p less than 0.01). These results suggest that the elevation of circulating ANP in hypertensives is involved in the pathogenesis of hypertension.
Atrial natriuretic peptide
Essential hypertension
Plasma renin activity
Pathogenesis
Plasma levels
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An association between aldosterone and insulin resistance has been demonstrated in obesity and primary aldosteronism and in blacks with the metabolic syndrome. The aim of this study was to evaluate the relationship of plasma aldosterone with insulin sensitivity in white subjects.In 356 patients with essential hypertension and 102 normotensive control subjects of comparable age and BMI, we measured, after discontinuation of treatment, plasma active renin, aldosterone, cortisol, glucose, insulin, and C-peptide levels and calculated markers of insulin sensitivity. Direct assessment of insulin sensitivity was obtained in a subset of 64 hypertensive patients by a hyperinsulinemic clamp.Hypertensive patients had significantly greater fasting plasma insulin and C-peptide concentrations and homeostasis model assessment (HOMA) indexes than normotensive control subjects. A positive association with increasing plasma aldosterone concentrations was demonstrated for plasma glucose, insulin, C-peptides, and HOMA. Assessment of insulin sensitivity by clamp showed a significant decrease of the metabolic clearance rate of glucose with increasing aldosterone levels. Significant correlations were found between plasma aldosterone, plasma insulin, and C-peptide levels, HOMA, and glucose metabolic clearance rate. Blood pressure and plasma potassium, plasma cortisol, and renin levels, but not BMI, were also directly correlated with plasma aldosterone. Multiple regression analysis showed that HOMA, together with plasma potassium, cortisol, and renin levels, was independently correlated with plasma aldosterone.This study demonstrates a direct relationship between aldosterone, insulin resistance, and hyperinsulinemia in white subjects. In patients with hypertension, this relationship might contribute to maintenance of high blood pressure and increased cardiovascular risk.
Hyperinsulinemia
Plasma renin activity
Essential hypertension
Glucose clamp technique
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Administration of a large dose of ACTH caused an acute increase in aldosterone excretion in normal subjects, in cases of uncomplicated essential hypertension and in primary aldosteronism. Plasma renin levels were unaltered. The continued administration of ACTH for several days led to a fall in aldosterone excretion to below the control value in most cases, even when the subjects were maintained on a low salt diet. On the day after ceasing ACTH treatment, aldosterone transiently fell to even lower levels, which were also inappropriate to the low sodium intake. These various changes in aldosterone excretion produced by ACTH administration cannot be explained by any concurrent changes in activity of the renin-angiotensin system. The data also suggest that any changes in electrolyte metabolism induced by ACTH are only a minor influence in causing the depression in aldosterone secretion which follows its initial rise. This second part of the biphasic response therefore appears to result from a direct effect of either ACTH or released glucocorticoid on the adrenal cortex. In 4 of 5 cases of primary aldosteronism, aldosterone excretion also exhibited a biphasic response to ACTH, and it was further depressed to normal levels after stopping the drug. These latter results indicate that the adrenal adenoma typical of primary aldosteronism is not completely autonomous of humoral influences.
Primary Aldosteronism
Plasma renin activity
Mineralocorticoid
Hyperaldosteronism
Essential hypertension
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Atrial natriuretic peptide
Plasma renin activity
Essential hypertension
Brain natriuretic peptide
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Plasma concentrations of angiotensin II (AII), aldosterone, 18‐hydroxycorti‐costerone and cortisol were measured in seven patients with benign essential hypertension and in seven age‐matched control subjects before, and at frequent intervals for 2 h after the intravenous injection of frusemide (40 mg). In the normal subjects, significant increases in the plasma levels of AII, aldosterone and 18‐hydroxycorticosterone were apparent from 15 min after diuretic administration. The integrated responses of each hormone to frusemide administration were calculated. Aldosterone and AII responses to the diuretic were closely related, although three hypertensive patients had normal integrated aldosterone responses despite subnormal increases in the plasma concentrations of AII. The integrated 18‐hydroxycorticosterone responses were greater in the hypertensive (median 970 nmol. h −1 . l −1 ) than in the normal subjects (median 180 nmol. h −1 . l −1 ), P < 0·05. Some patients with a raised blood pressure appear to have an enhanced adrenal corticosteroid response to frusemide; this probably reflects an increased sensitivity to angiotensin II.
Essential hypertension
Mineralocorticoid
Plasma renin activity
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Aldosterone and 18–hydroxycorticosterone (18–OHB) are produced by the adrenocortical zona glomerulosa. Under normal conditions, plasma 18–OHB levels parallel and are influenced by the same trophic factors that regulate aldoste-rone production. To evaluate corticosterone-methyl-oxidase II activity, the final step of aldosterone biosynthesis, in conditions associated with chronic derangements of the pituitary-adrenal and/or renal-adrenal axis, we measured the plasma 18–OHB to aldosterone ratio, cortisol, PRA or plasma renin concentration, and potassium (K) in 104 such patients and 15 normal subjects. The 18-OHB to aldosterone ratios in the pituitary-adrenal group were not significantly different from normal regardless of elevated or reduced ACTH and/or cortisol levels [patients with Cushing's syndrome, 3.55 ± 0.68 (±SE); ACTH deficiency, 2.03 ± 0.34; 21-hydroxylase deficiency, 3.09 ± 0.23; normal subjects, 2.50 ± 0.15]. The renal-adrenal group also had normal ratios regardless of plasma renin concentration and K levels [patients with aldosterone-producing adenomas, 2.85 ± 0.15; idiopathic hyperaldosteronism, 2.14 ± 0.19; salt-losing nephropathy, 3.06 ± 0.54; Bartter's syndrome, 2.89 ± 0.20; isolated (hyporeninemic) hypoaldosteronism, 3.20 ± 0.39]. Only in patients with 17a-hydroxylase deficiency (230.1 ± 118.6) was the ratio abnormally high. Chronic perturbations of aldosterone production by ACTH, the renin-angiotensin system, and/or K did not alter this last step of aldosterone biosynthesis (corticosterone-methyl-oxidase II), as defined by their plasma concentrations. Any influence of these trophic factors must be proximal to the site of 18-OHB production.
Corticosterone
Plasma renin activity
Mineralocorticoid
Hyperaldosteronism
Essential hypertension
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Citations (32)