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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of caffeine on blood cortisol levels and blood pressures was examined during rest and in response to a challenging psychomotor task in men with a low versus high risk of essential hypertension. Thirty-four healthy men ages 21-35 years were selected such that 17 were at high risk for hypertension (positive parental history and screening blood pressures of 135/85-155/95 mm Hg) and 17 were at low risk (negative parental history and no pressures above 132/84 mm Hg). Testing consisted of quiet rest (20 minutes); oral placebo (grapefruit juice) or caffeine administration (3.3 mg/kg in grapefruit juice); rest during a postdrug absorption period (40 minutes); work on an unsignalled simple reaction time task (15 minutes); and quiet rest (20 minutes). Blood pressures were recorded at 2-minute intervals, and blood samples were withdrawn via an indwelling catheter at the end of the baseline, drug absorption, task, and recovery periods. The combination of task plus caffeine produced the highest blood pressures in men at risk for hypertension. Cortisol levels were found to be sustained during rest in members of the high risk group after they had consumed caffeine, whereas members of the low risk group showed a modest decline. The high risk subjects also showed a significant rise in cortisol during (+3.7 micrograms/dl) and after (+4.0 micrograms/dl) work on the reaction time task after caffeine consumption.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1989 Aug
PMID:Caffeine may potentiate adrenocortical stress responses in hypertension-prone men. 254 9

Effects of chronic glucocorticoid treatment on arterial baroreflex function and on cardiac beta- and vascular alpha-adrenoceptor-mediated responses were assessed in conscious, unrestrained Wistar-Kyoto rats. Cortisol (25 mg/kg/day) was administered for seven days using a subcutaneous reservoir pump. Arterial baroreflex-cardiac sensitivity was assessed by examining the relationship of the cardiac interbeat interval to the mean arterial blood pressure during phenylephrine or nitroprusside challenge; baroreflex-sympathoneural sensitivity was assessed from the ratio of the increase in the arterial norepinephrine concentration to the decrease in mean arterial pressure at 15 min during intravenous infusion of nitroprusside; cardiac beta-adrenoceptor-mediated responsiveness was estimated from heart rate responses to bolus-injected isoproterenol; and vascular alpha-adrenoceptor-mediated responsiveness was estimated from peak mean arterial pressure responses to bolus-injected phenylephrine. Cortisol treatment increased mean arterial pressure, decreased heart rate, and increased heart rate responses to isoproterenol, whereas baroreflex-vagal sensitivity, baroreflex-sympathoneural sensitivity, and pressor responses to phenylephrine were unaffected. The results indicate that hypertension due to chronic cortisol administration is not associated with decreased sensitivity of the baroreceptor-cardiac reflex. Baroreflex-sympathoneural sensitivity and alpha 1-adrenoceptor responsiveness also remain normal, whereas beta-adrenoceptor responsiveness is increased. The findings suggest that the pattern of neurocirculatory adjustment in glucocorticoid hypertension differs from that seen in other forms of hypertension.
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PMID:Neurocirculatory regulation in cortisol-induced hypertension. 255 18

Ketoconazole, an oral antimycotic agent, is known to have a potent inhibitory effect on adrenal steroid production. It was given at a dose of 1200 mg/day to a 52-year-old female patient with a virilizing adrenocortical carcinoma in order to achieve better metabolic control pre-operatively. Together with a rapid normalisation of hypertension and hyperglycemia, a dramatic fall was noticed in serum and urinary adrenal steroids after a few days. Levels of total testosterone (20 nmol/l), androstenedione (greater than 35 nmol/l) and DHEA-sulphate (greater than 28 nmol/l) fell to normal levels in 6 days. By contrast, levels of 17-OH-progesterone (30 nmol/l) and progesterone (2.45 nmol/l) increased slightly, indicating inhibition of adrenal 17,20-lyase. Cortisol (620 nmol/l at 08.00 h) fell to very low levels (50 nmol/l) on day 6 of the trial. We conclude that ketoconazole is very effective in suppression of adrenal tumoural steroidogenesis and merits consideration in pre-operative use. We warn against dangerous hypoadrenalism which seems to occur earlier in tumoural than in normal adrenal metabolism.
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PMID:Use of ketoconazole in the treatment of a virilizing adrenocortical carcinoma. 277 22

Carbenoxolone Sodium (CS), a chemical derivative of liquorice is known to be associated with hypertension, increased sodium retention and hypokalemia. The present studies describe the effects of CS on the renal actions of the glucocorticoids Corticosterone (B) and Cortisol (F) on sodium and potassium in adrenalectomized male rats. B (50, 100 and 500 micrograms/rat) and F (1 mg/rat) were found to possess no intrinsic antinatriuretic activity which is represented by a decrease in the Na+ to creatinine ratio; while only B (500 micrograms/rat) demonstrated kaliuretic effects as indicated by an increase in K+ to creatinine ratios. B and F showed very significant antinatriuretic and kaliuretic properties following pretreatment with CS (2.5 mg/rat). CS alone was not found to be antinatriuretic at this dosage. Further experiments demonstrated that lower dosages of CS (500 and 1,000 micrograms/rat) also cause B to exhibit Na+ retaining and K+ excreting properties. Thus, we have demonstrated that pretreatment with CS can confer mineralocorticoid-like activity upon the glucocorticoids B and F.
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PMID:The antinatriuretic and kaliuretic effects of the glucocorticoids corticosterone and cortisol following pretreatment with carbenoxolone sodium (a liquorice derivative) in the adrenalectomized rat. 291 28

Hydrocortisone and aldosterone concentration was determined in 138 patients with arterial hypertension of adrenal and renal genesis in the blood of the adrenal veins and in the cistern of the vena cava inferior, that of deoxycorticosterone in 50 patients, ACTH in 51 and renin activity in the blood plasma of the renal veins in 21 patients. The concentration of steroid hormones adequately reflected adrenal cortex function facilitating differential diagnosis between renal and adrenal pathology variants. Differential diagnostic analysis on the basis of change in the concentration of steroid hormones was found difficult or impossible if the patients received steroidogenesis changing drugs on day, preceding veno graphic examination of the adrenals.
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PMID:[Hormone levels of the blood of the adrenal veins and inferior vena cava in patients with adrenal and kidney diseases]. 299 98

Dexamethasone-suppressible hyperaldosteronism is a rare familial syndrome in which hypokalemia, suppression of plasma renin concentration, and elevated aldosterone secretion are corrected by treatment with glucocorticoids. Regulation of adrenocortical function and body electrolytes was studied in two affected brothers. Both were hypertensive (210/128 and 160/106 mm Hg) with hypokalemia (3.3 and 3.5 mM) and low plasma renin concentrations. Aldosterone was elevated intermittently with levels as high as 45 ng/dl (normal range, 4-16 ng/dl). Cortisol concentrations were normal but were correlated with aldosterone levels (r = 0.9 and 0.7). Concentrations of 11-deoxycorticosterone (19 and 21 ng/dl; normal range, 4-16 ng/dl) and 18-hydroxycortisol (1000 and 950 ng/dl; normal range, 34-150 ng/dl) were elevated, and diurnal changes in both were the same as those seen with aldosterone. Infusion of adrenocorticotropic hormone (ACTH) caused exaggerated increases of aldosterone, 11-deoxycorticosterone, and 18-hydroxycortisol; cortisol response was normal. A 4-week trial of dexamethasone normalized blood pressure and caused a natriuresis, a fall in aldosterone, and a rise in plasma renin. Administration of ACTH after dexamethasone treatment again caused exaggerated increases of aldosterone. Aldosterone did not respond to angiotensin II before dexamethasone therapy (r = 0.01), but it showed a normal response after therapy (r = 0.8, p less than 0.01). Neither administration of dopamine (1 microgram/kg/min) nor long-term therapy with bromocriptine (2.5 mg t.i.d. for 4 weeks) affected aldosterone biosynthesis. Thus, loss of dopaminergic inhibition of mineralocorticoid biosynthesis does not account for hyperaldosteronism in this condition.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1986 Aug
PMID:Dexamethasone-suppressible hyperaldosteronism. Adrenal transition cell hyperplasia? 301 96

Cortisol 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD) deficiency was observed in four patients with apparent mineralocorticoid excess. The 11 beta-HSD deficiency was demonstrated by a markedly decreased urinary tetrahydrocortisone/tetrahydrocortisol (THE/THF) ratio (less than 1 in normal children) during infusion of ACTH and administration of hydrocortisone. We propose that in these patients the 11 beta-HSD deficiency impairs the metabolism of cortisol to cortisone, resulting in a prolonged cortisol half-life, suppression of ACTH, and normal serum cortisol. The 11 beta-HSD deficiency protects the patient from adrenal insufficiency despite the low cortisol secretion; the prolonged half-life of cortisol may contribute to the hypertension and hyporeninemia observed in this disorder. Continuous intravenous hydrocortisone administration resulted in increased blood pressure and decreased serum potassium. Addition of spironolactone during continued administration of 20 mg per day of hydrocortisone resulted in a decrease in blood pressure and a rise in serum potassium. These studies suggest that an abnormality in cortisol action or metabolism results in cortisol behaving as a potent mineralocorticoid. These findings may account for this syndrome of apparent mineralocorticoid excess.
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PMID:Apparent mineralocorticoid excess causing hypertension and hypokalemia in children. 346 39

Glucocorticoid induced hypertension has been regarded as independent of sodium (Na), in contrast to mineralocorticoid induced hypertension, which is Na+-dependent. These studies compare the effect of Na+ depletion and potassium (K+) loading on glucocorticoid hypertension induced by cortisol in conscious sheep. Cortisol (480 mg/d) for 5 days, in sheep on a normal chaff diet (90-140 mmol/d Na+, 200-250 mmol/d K+) increased mean arterial pressure by 18 mmHg on day 5, increased plasma Na+ concentration, reduced plasma K+ concentration, and did not change urinary Na+ excretion. Following Na+ depletion (Na+ loss 603 +/- 49 mmol), cortisol increased mean arterial pressure from 70 +/- 1 mmHg to 76 +/- 3 mmHg on day 5 (P less than 0.001) and the increase in pressure was significantly less than the increase seen on the normal diet (P less than 0.05). Plasma Na+ increased and plasma K+ decreased. Urinary Na+ and K+ excretion was unchanged. KCl loading (700-900 mmol/day) for 10 days had no effect on the maximum rise in mean arterial pressure (+18 mmHg with cortisol in K+ loaded sheep). Plasma Na+ and K+ fell, and urinary Na+ excretion increased during the infusion. These studies show that Na+ depletion, but not KCl loading, reduced cortisol induced hypertension in sheep. These data show that glucocorticoid hypertension is not independent of Na+ status.
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PMID:The effect of sodium depletion and potassium loading on cortisol induced hypertension in sheep. 377 38

A 26-yr-old woman presented with hirsutism, male pattern scalp baldness ("geheimratsecken"), and menstrual irregularities. She had no hypertension or other signs and symptoms of Cushing's syndrome. Plasma cortisol levels were greatly elevated and did not suppress normally in response to dexamethasone. Cortisol binding to transcortin was normal. Plasma androstenedione and testosterone levels were also increased, but 17-hydroxyprogesterone and aldosterone levels were normal. Further studies revealed an increased cortisol production rate, increased 24-h urinary cortisol excretion, increased plasma ACTH levels, a normal diurnal rhythm of cortisol at an elevated level, and normal increments of plasma ACTH, cortisol, GH, and PRL in response to insulin-induced hypoglycemia. The father and two brothers also had increased plasma cortisol levels, which did not suppress normally in response to dexamethasone. Chronic therapy with dexamethasone (at first 1 and later 0.5 mg, three times daily) for more than 30 weeks resulted in decreased hirsutism, normalization of scalp hair and menstrual cyclicity, and normal plasma testosterone and androstenedione levels. No signs or symptoms of Cushing's syndrome developed, and the central regulation of secretion of ACTH, cortisol, GH, and PRL (insulin test, diurnal rhythm) remained qualitatively normal at a lower set-point. We conclude that this patient had autosomal dominantly inherited hereditary (partial) cortisol insensitivity, which had resulted in increased adrenocortical cortisol and androgen secretion. The latter had not resulted in clinical symptoms in the three afflicted male members of the family, but had in the propositus. The results also indicate the potential usefulness of the insulin test in distinguishing this disorder from Cushing's disease.
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PMID:Familial cortisol resistance: differential diagnostic and therapeutic aspects. 378 21

Primary cortisol resistance in man is a familial disease. It is characterized by increased plasma cortisol concentrations, high urinary free cortisol excretion, a normal circadian pattern of cortisol secretion, resistance to adrenal suppression by dexamethasone and absence of clinical stigmata of Cushing's syndrome. In its severe form, hypertension and hypokalemic alkalosis are present, owing to increased secretion of the sodium-retaining corticoids, corticosterone and deoxycorticosterone. In subjects with a less severe resistance to cortisol, there are no clinical abnormalities and the disease is revealed only by detailed examination of several parameters of cortisol metabolism. In the whole-cell assay (peripheral mononuclear leukocytes or fibroblasts) the glucocorticoid receptor shows a low affinity for dexamethasone. The receptor may be unsaturable as suggested by decreased receptor concentrations in broken-cell systems. Thus, generalized target-tissue resistance to cortisol, including the pituitary gland and the hypothalamus, is accompanied by a decreased negative feedback of the cortisol-ACTH feedback system resulting in increased ACTH secretion. This causes higher plasma cortisol to compensate for the end-organ resistance and also increases the production of adrenal mineralocorticoids, as by-products. Thus hypertension and hypokalemic alkalosis depends on the degree of the resistance. Cortisol resistance in many New World primate species is characterized by greatly increased plasma cortisol concentrations, decreased cortisol binding globulin capacity and affinity, high levels of plasma and urinary free cortisol, marked resistance of ACTH suppression by dexamethasone, and no physiologic evidence of glucocorticoid hormone excess. Target tissues have normal concentrations of glucocorticoid receptors with decreased affinity for dexamethasone. The New World primates, unlike man, have compensated for this cortisol resistance with intra-adrenal adaptations over the 50 million years of their evolutionary development. These primates also have abnormalities of other steroid hormone-receptor systems such as progesterone, estrogen, androgen and mineralocorticoid. In contrast, the human syndrome appears to be a recent mutation with pathophysiologic consequences.
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PMID:Primary cortisol resistance: a familial syndrome and an animal model. 688 85


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