[Behavior of aldosterone and plasma renin activity after ACTH administration and insulin-induced hypoglycemia in patients with essential arterial hypertension].
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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.Keywords:
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Insulin-induced hypoglycemia caused an increase in plasma aldosterone as well as in renin activity and cortisol. After the suppression of the renin-angiotensin system by the prior administration ol propranolol, insulin-induced hypoglycemia still caused a significant increase in plasma aldosterone similar to the increase in plasma cortisol, though plasma renin activity was suppressed. Conversely, after the suppression of endogenous ACTH by the prior administration of dexamethasone, insulin-induced hypoglycemia failed to induce a rise in plasma aldosterone and plasma cortisol, though plasma renin activity increased. The increase of plasma aldosterone in response to exogenous ACTH was not different with or without the prior administration of dexamethasone. We conclude that ACTH is largely responsible for the increased aldosterone secretion after insulininduced hypoglycemia.
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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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The responsiveness of plasma aldosterone to the infusion of angiotensin II at dose rates of 2, 4, and 10 ng/kg- min was assessed in 11 normal subjects and i3 patients with mild essential hypertension before and after 4 weeks of treatment with the sympatholytic agent debrisoquine. Debrisoquine treatment caused a significant (P < 0.01) decrease in circulating norepinephrine (−45%), but did hot modify plasma levels of angiotensin II, renin, aldosterone, or epinephrine or the metab- olism of sodium or potassium. In normal subjects, debrisoquine caused a significant shift to the left (P < 0.05) of the correlation relating plasma aldosterone to plasma angiotensin II levels. In patients with essential hypertension, the aldosterone-angioten-sin II interrelationship was not modified. These findings suggest that the sympathetic nervous system exerts an inhibitory influence on aldosterone responsiveness to angiotensin II in normal man, and that this physiological interaction is impaired in patients with essential hypertension.
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Plasma renin activity
Mineralocorticoid
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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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Low renin essential hypertensives (LRH) have normal plasma aldosterone levels which are inappropriately high in relation to their PRA. Posture is the major determinant for plasma aldosterone and PRA levels, but it is not known whether postural increments (Δ) of plasma aldosterone and (Δ) PRA are also abnormal in LRH. To evaluate this, LRH (n = 8), normal renin hypertensives (NRH; n = 9), normotensive controls (n = 18), and subjects with idiopathic hyperaldosteronism (IHA; n = 5) were studied in a metabolic unit on a controlled diet over 7 days. Overnight supine and 4-h upright PRA, plasma aldosterone, and 24-h urinary tetrahydroaldosterone (THA) and aldosterone secretion rates (ASR) were measured. The Δ in plasma aldosterone after 4 h of upright posture was not different in the four groups. The ratio of A plasma aldosterone/Δ PRA, however, was elevated in both IHA and LRH compared to that in NRH and normals. THA excretion was also elevated in IHA and LRH, but LRH had a normal ASR. This resulted in a higher fractional THA excretion (THA/ASR) in LRH compared to the other three groups. These data further support enhanced adrenal angiotensin-II sensitivity in LRH. Aldosterone was preferentially metabolized to THA in LRH. Since THA has reduced biological activity, this may be a compensatory mechanism to reduce mineralocorticoid activity in LRH.
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Hyperaldosteronism
Essential hypertension
Supine position
Mineralocorticoid
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30% of patients with essential hypertension have a decreased adrenal response to angiotensin II (A II) on a low but not a high sodium intake. They also have a compensatory increase in the activity of the renin-angiotensin system best documented in a sodium-restricted state.
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Plasma aldosterone (PA), plasma renin activity (PRA), extracellular fluid volume (EFV) and hepatic blood flow were measured in forty-four patients with sustained essential hypertension and compared with forty-two normotensive controls of same age and sex. All patient had inulin clearances within the normal range and balanced sodium intake and urinary output. In hypertensives, PA, PRA, EFV and hepatic blood flow were within normal ranges; the log-ratio PA:PRA was significantly elevated (P less than 0.001). In normotensives, a negative relationship was observed between PA and EFV (r=-0.55; P less than 0.001) while a positive relationship was observed between PA and PRA (=+0.70; P less than 0.001). In hypertensives, the two relationships were disrupted or less significant: for a given value of EFV, PA was more elevated in hypertensives than in normotensives; for a given value of PRA, PA was more evaluated in hypertensives than in normotensives. The results could not be explained on the basis of a disturbance in hepatic blood flow and/or in the metabolic clearance rate of aldosterone. The study provided evidence that, in patients with sustained essential hypertension and equilibrated sodium balance, there is an excess of plasma aldosterone relative to the levels of extracellular fluid volume and plasma renin activity. The excess of probably related to an abnormality in the adrenal secretion.
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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.
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