Elevated Serum Aldosterone Levels in Patients with Psoriasis and Systemic Arterial Hypertension: A Cross-Sectional Study
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Abstract Background Epidemiological studies suggest a higher prevalence of systemic arterial hypertension (HTN) and other cardiovascular diseases in patients with psoriasis. The underlying mechanism remains unclear, but may involve activation of the renin-angiotensin-aldosterone system (RAAS). This study aimed to compare renin and aldosterone levels between psoriasis patients and non-psoriasis individuals. Methods: A prospective, cross-sectional study enrolled consecutive patients from a university hospital’s dermatology outpatient clinic. Clinical evaluation was followed by blood collection for renin and aldosterone measurement, allowing for comparison between psoriasis and non-psoriasis patients. Subgroup analyses stratified participants based on HTN presence. Multiple linear regression analyses identified independent predictors of higher renin and aldosterone levels. Results: The study included 170 patients (mean age: 55 ± 13 years, 50.6% men, 85.9% non-white), 57.6% having psoriasis and 44.1% having HTN. Mean plasma renin levels were similar in psoriasis and non-psoriasis patients (26.3 ± 51.4 versus 23.9 ± 48.7 µUI/ml, respectively, p = 0.764). However, psoriasis patients showed significantly higher mean serum aldosterone levels (25.3 ± 49.4 versus 11.7 ± 10.7 ng/dl, p = 0.009). Stratification revealed that only psoriasis patients with HTN had significantly higher aldosterone levels compared to other subgroups. In multiple linear regression analyses, psoriasis was only associated with higher levels of aldosterone in hypertensive patients. Conclusions: This study indicates elevated serum aldosterone levels in patients with psoriasis and HTN. Further investigation is necessary to understand the potential impact of this finding on cardiovascular morbidity and mortality in psoriasis patients.Keywords:
Plasma renin activity
Cross-sectional study
Outpatient clinic
Primary Aldosteronism
The effects of standard oral glucose loading (100 g) on plasma aldosterone and some regulatory factors were assessed in patients with primary hyperaldosteronism and normal subjects. Following overnight fast, mean plasma glucose was identical (10 patients and normal subjects approximately matched per age and sex); plasma insulin, potassium and renin levels were lower and plasma aldosterone higher in the patients. Glucose loading significantly increased plasma glucose and insulin concentrations and decreased plasma potassium and aldosterone levels in both groups; plasma renin activity was significantly increased only in normal subjects. The increases in plasma insulin and the decreases in plasma potassium or aldosterone tended to be blunted in primary hyperaldosteronism. Relationships among glucose-induced changes in plasma aldosterone and other factors were assessed by multiple regression analysis in these patients and normal subjects as well as an additional group of 21 normal subjects; in the latter, plasma cortisol was also measured and found to decrease significantly after glucose loading. Changes in plasma aldosterone correlated (P less than 0.025) more closely with those in plasma potassium in the patients and with variations in plasma renin activity in the normal subjects. These findings suggest that complex metabolic changes occur following glucose ingestion which are capable of modifying aldosterone secretion in normal subjects and primary hyperaldosteronism. The aldosterone-inhibitory effect of glucose tends to be blunted in the latter disorder. This could be related at least in part to an impaired insulin response in primary hyperaldosteronism.
Hyperaldosteronism
Plasma renin activity
Mineralocorticoid
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The patient was admitted to our hospital at 19 and again at 22-yr of age for hirsutism and hypertension. Her baseline and ACTH-stimulated plasma 17-hydroxy pregnenolone, dehydroepiandrosterone and dehydroepiandrosterone sulfate were increased whereas plasma 17-hydroxy progesterone and androstenedione were normal and responded poorly to ACTH. Plasma deoxycorticosterone, corticosterone and cortisol baseline levels were normal, and they responded normally to ACTH. The plasma aldosterone concentration (PAC) was always high and responded well to ACTH, angiotensin III and furosemide-upright stimulation. However, plasma renin activity (PRA) was normal or slightly high, and responded normally to furosemide-upright stimulation and fluorohydrocortisone suppression. Dexamethasone (2mg/day) for 1-2 weeks suppressed the androgens, cortisol and corticosterone levels. PRA and PAC were suppressed temporally, but PRA returned to normal and PAC to be a high level after 2 weeks of dexamethasone administration. Blood pressure was also reduced temporally but returned to a high level after 2 weeks of dexamethasone. These results indicate that primary aldosteronism and dexamethasone-suppressible hyperaldosteronism were not likely to be present, and unkown aldosterone stimulating factors which potentiated the action of endogenous angiotensin II or ACTH might be responsible for the hyperaldosteronism in this patient. We conclude that this patient had a mild and non-salt losing 3β-HSD deficiency in the zona reticularis with normal fasciculata and high glomerulosa function.
Zona fasciculata
Hyperaldosteronism
Plasma renin activity
Primary Aldosteronism
Bartter's syndrome
Mineralocorticoid
Corticosterone
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In dogs injected for 5 days with dog renin, then hypophysectomized and nephrectomized, the increments in aldosterone output produced by ACTH and angiotensin II were found to be greater than in noninjected control dogs. This increase resembles that seen in dogs fed a low sodium diet, which also increases renin secretion. The increments in 17-hydroxycorticoid secretion produced by angiotensin II and ACTH were unchanged by the renin treatment. There was no adrenocortical hypertrophy, sodium diuresis, or change in plasma sodium in the renintreated dogs, although plasma potassium fell significantly. The results support the hypothesis that the increase in the aldosterone-stimulating activity of ACTH and angiotensin II seen in dogs fed a low sodium diet is produced by the increase in circulating renin levels. (Endocrinology 80: 703, 1967)
Plasma renin activity
Low sodium diet
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The upright and supine circadian rhythms of plasma renin activity (PRA), plasma aldosterone (PA), plasma cortisol (PC), and serum growth hormone (GH) were determined in 7 normals and 12 patients with hypertension, low PRA, and normal aldosterone excretion (LRH = low renin hypertension). In general PRA was always lower in LRH than in normals. However, PA in LRH was essentially normal. The average PC was greater in LRH than in normals and there were some differences between normals and LRH in the circadian rhythm of PC. Levels and patterns of growth hormone were not different between the two groups. A probable circadian rhythm of plasma aldosterone was demonstrated in normals and in LRH both in the upright and recumbent positions. Under these circumstances the higher plasma aldosterone noted in the morning than in the evening was not associated with changes in the mean circulating levels of PRA. However, significant decreases in PC were found from morning to evening. This suggests a possible role for ACTH in the control of aldosterone production not only in normals but also in patients with LRH. However, the factor maintaining normal aldosterone production in LRH does not appear to be either PC or GH. Unusual sensitivity of the adrenal gland to circulating levels of PRA may be at least partially responsible since PRA and PA were highly correlated. Finally, during prolonged recumbency, PRA and PC in normal subjects were similar to values in LRH, but PA was clearly greater than normal, demonstrating higher aldosterone levels in LRH compared to normals.
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SUMMARY Diurnal studies were performed on ten normal volunteers taking a normal sodium diet. Half‐hourly blood samples were taken throughout 25 h and assayed for plasma renin activity (PRA) and the plasma concentrations of noradrenaline, aldosterone and cortisol. Sleep was recorded polygraphically and scored by standard criteria. Circadian rhythms were demonstrated for plasma cortisol, aldosterone and noradrenaline concentrations, but not for plasma renin activity. The nadir of the rhythm for the noradrenaline concentration appeared to be related to sleep itself rather than to any chronological index. Only PRA was effected by the stage of sleep, falling sharply during periods of REM sleep. Plasma cortisol and aldosterone concentrations showed a positive correlation over the 24 h. There was, however, no correlation between PRA and plasma aldosterone concentrations, except when the subjects arose after their night's recumbency. Plasma noradrenaline concentration did not correlate with the concentration of any of the other hormones measured.
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SUMMARY Recent investigations suggest that dopamine inhibits aldosterone secretion. To test the hypothesis that dopamine contributes to the reduced aldosterone secretion on a high sodium intake, eight normal subjects were studied in metabolic balance on both 200 and 10 mmol sodium diets. On each diet, the subjects received a constant 4 h intravenous infusion of the dopamine antagonist, metoclopramide (MCP). Although MCP significantly increased plasma aldosterone (PA) throughout the infusion on both diets, the maximum increment in PA was greater on the low (37 ± 5 ng/dl) than on the high (14 ± 4 ng/dl) sodium intake ( P <0·02). The greater response on the low sodium intake could not be ascribed to changes in potassium, cortisol or ACTH. However, plasma renin activity (PRA) and angiotensin II (AII) levels were significantly ( P <0·01) increased by MCP while on the low but not the high sodium intake. We conclude that the rise in PA while on a high sodium intake reflects dopaminergic antagonism by MCP directly at the level of the adrenal gland. On the low sodium intake, the enhanced PA response to MCP probably reflects both a direct adrenal effect and an indirect effect mediated via activation of the renin‐angiotensin system.
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To evaluate the interrelationship between plasma aldosterone (PA) and dopamine (DA) in primary aldosteronism we determined their correlations during nycthemeral cycles (before and after dexamethasone), as well as during postural or episodic increases in PA in four patients. Plasma cortisol and PRL were also determined. There was an overall negative correlation between plasma DA on the one hand and PA, PRL, and cortisol on the other, the latter three being positively correlated with one another. The strongest positive relationship was between aldosterone and cortisol; the strongest negative correlation was between PRL and free DA. Dexamethasone administration suppressed PA to 70 ± 6%, PRL to 71 ± 5%, and cortisol to 24 ± 2% of the previous levels (100%), and increased plasma free DA to 260 ± 49%. During the first 12 h ofthe cycle, corresponding to PA suppression by dexamethasone, the positive correlation between PA and plasma cortisol strengthened, and a positive correlation of plasma cortisol with PRL appeared; both disappeared in the second 12 hcorresponding to the escape of PA from the inhibitory action of dexamethasone. In a patient with periodic hyperaldosteronism in 8– to 10-day cycles, lower PA and normokalemia were associated with a huge increase in plasma conjugated DA; when plasma conjugated DA was low, it was associated with high PA and low potassium levels. The observation of elevated plasma DA suggests that the dopaminergic inhibitory pathway of aldosterone is activated in primary aldosteronism. Opposing fluctuations in PA, PRL, and cortisol on the one hand and plasma DA on the other, spontaneously or during dexamethasone administration, are compatible with the hypothesis that a weakening of dopaminergic inhibitory control contributes to the otherwise unexplained PA surges, while an increase in DA contributes to the dexamethasoneinduced suppression of PA; the positive correlation of plasma cortisol with PA and PRL suggests that this inhibitory action of DA may be mediated in the first 12 h by suppression of ACTH secretion but later may act independently of it.
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Hyperaldosteronism
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The control of aldosterone secretion was investigated in 23 hyperthyroid patients. Compared to normal subjects, chronically sodium restricted hyperthyroid patients had blunted aldosterone secretion (645 ± 73 μg/day); low plasma aldosterone (47 ±4 ng/100 ml); increased estimated aldosterone metabolic clearance rate (2230 ± 284 L/day); and increased plasma renin activity (32.7 ± 3.5 ng/ml/3 hr). Renin and aldosterone responses during ACTH and saline loading were normal, and oral potassium loading normalized aldosterone secretion and lowered renin activity. Propranolol significantly lowered renin activity but not aldosterone secretion. The elevated plasma renin activity was probably secondary to increased sympathetic stimulation and potassium depletion. It is likely that potassium depletion also contributed to the blunted aldosterone secretion during sodium deprivation.
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Large doses of atrial natriuretic peptide (ANP) inhibit renin and aldosterone secretion in normal man, but the effect of physiological levels is unknown. We, therefore, studied the effect of a low infusion rate of alpha-human ANP (alpha hANP; 0.5 microgram/min for 180 min) on the plasma corticosteroid response to graded physiological doses of angiotensin II (0.5, 1.0, 2.0, and 4.0 ng/kg X min, each for 30 min) and ACTH (6.25, 12.5, 25, and 50 mIU, each for 30 min) in six normal men eating a low salt diet (10 mmol sodium and 100 mmol potassium daily). The angiotensin II and ACTH infusions were given from 0900-1100 h on separate days, during which randomized infusions of placebo or alpha hANP were given from 0800-1100 h according to a single blind protocol. Plasma immunoreactive ANP levels were less than 10 pmol/L on the placebo day compared to 30-50 pmol/L during the alpha hANP infusions, and were not altered by either ACTH or angiotensin II. Compared with the control observations, there was no significant change in arterial pressure or heart rate during either the alpha hANP or angiotensin II infusions. ACTH infusions evoked an incremental response in plasma aldosterone and cortisol, and the dose-response relationship was unaltered by alpha hANP. In contrast, while an incremental and significant increase in plasma aldosterone in response to angiotensin II occurred with the placebo infusion, no significant increase occurred in response to angiotensin during the alpha hANP infusion. The slope of the angiotensin II/aldosterone regression line was significantly less during all alpha hANP infusions compared to that during the placebo infusion (P less than 0.02). In addition, on the ACTH infusion day significant suppression of both PRA (P less than 0.05) and plasma angiotensin II (P less than 0.008) occurred during the alpha hANP infusion compared to that during the placebo infusion, whereas PRA was equally suppressed by angiotensin II in the presence or absence of alpha hANP. alpha hANP also increased urine volume [176 +/- 31 (+/- SEM) vs. 113 +/- 19 mL/mmol creatinine with placebo; P less than 0.03] and sodium excretion (2.14 +/- 0.48 vs. 0.58 +/- 0.22 mmol/mmol creatinine with placebo; P less than 0.004) on the ACTH infusion days. With angiotensin II, urine volume was also significantly increased by alpha hANP (150 +/- 27 vs. 81 +/- 15 mL/mmol creatinine with placebo; P less than 0.03), and urine sodium excretion doubled.(ABSTRACT TRUNCATED AT 400 WORDS)
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The plasma and adrenal renin-angiotensin system in stroke-prone spontaneously hypertensive rats (SHRSP) and Wistar-Kyoto (WKY) rats were examined in animals at 5, 11, 18, and 25 weeks of age. Plasma active renin was significantly increased in 18- and 25-week-old SHRSP with impaired renal function, whereas there was no difference in the plasma prorenin level or renal renin content between the two strains at all ages examined. Thus, the rate of activation of prorenin seems to be enhanced in the kidney of SHRSP with malignant hypertension. Adrenal renin contents were severalfold higher in SHRSP than WKY rats at all ages. However, adrenal angiotensin peptides were not increased in SHRSP aged 5 and 11 weeks. In 18-week-old SHRSP, adrenal angiotensin II (Ang II) and III (Ang III) levels were fourfold and 1.8-fold higher, respectively, than in WKY rats, accompanied by 1.5-fold higher plasma aldosterone. Increased adrenal angiotensin and plasma aldosterone were also found in 25-week-old SHRSP. Zonal distribution studies indicated that the elevated Ang II and III in SHRSP were derived mainly from the capsular tissue (the zona glomerulosa). To examine the contribution of circulating angiotensin to the adrenal angiotensin content, effects of bilateral nephrectomy on adrenal angiotensin and renin were examined in 18-week-old rats. At 24 hours after nephrectomy, plasma angiotensin, prorenin, and active renin were decreased to almost negligible concentrations. Conversely, in both adrenal capsular and decapsular tissues of SHRSP and WKY rats, neither angiotensin nor renin was significantly decreased after nephrectomy. These results suggest that the increase in adrenal capsular Ang II contents in SHRSP may be partly due to an enhanced local production of Ang II.
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Angiotensin III
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