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

Hypertension, hypokalemia, suppressed plasma renin activity and increased plasma aldosterone were found in a middle-aged woman. Following removal of the tumor in the left adrenal gland these abnormalities disappeared. Concurrently, however, the plasma cortisol level did not show normal diurnal change, although the value at 6 A.M. was within the normal range. Administration of 2 mg dexamethasone failed to depress the plasma cortisol level and urinary 17-OHCS concentrations. Postoperatively, plasma cortisol and urinary 17-OHCS were below normal. Histologic examination of the tumor indicated the presence of two types of adenoma cells; one was a large watery clear cell with rich lipid and possibly with aldosterone secretion and the other was an acidophilic cell with poor lipid and possibly with cortisol secretion. It is suggested that, in addition to oversecretion of aldosterone, the tumor autonomously secreted cortisol, although the amount of cortisol secreted was not large enough to produce typical Cushing's syndrome.
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PMID:Concurrent hypersecretion of aldosterone and cortisol from the adrenal cortical adenoma. 47 99

Adrenal steroids and compenents of the renin-angiotensin system were measured before and after adrenalectomy in a woman with Cushing's syndrome and hypertension from a functioning adrenocortical adenoma. Aldosterone, deoxycorticosterone and cortisol were produced in excess by the adenoma, and were measured in tumor tissue. High plasma renin substrate concentrations, and normal basal and furosemide-stimulated plasma renin activities and plasma renin concentrations which were present before surgery, decreased after adrenalectomy, and the hypertension diminished. The inappropriately normal levels of renin and potassium in this patient, despite autonomous aldosterone overproduction, suggest an ineffective mineralocorticoid action of aldosterone, possibly from interaction with her other adenoma-produced steroids. The decrease in components of the renin-angiotensin system suggests a partial renin-dependence of her hypertension.
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PMID:Hypertension and aldosterone overproduction without renin suppression in Cushing's syndrome from an adrenal adenoma. 47 1

Computarized axial tomography has shown the localization of adrenal lesions in four cases of hypertension of adrenal origin: two phaeochromocytomas, one primary hyperaldosteronism, one Cushing's syndrome. This method has the advantage of being neither invasive, nor time-consuming. Unfortunately, it cannot localize tumors smaller than two cm in diameter. It seems to be highly beneficial in phaeochromocytoma, where it can advantageously take the place of arteriography. It is less fruitful in primary hyperaldosteronism and in Cushing's syndrome because lesions are smaller.
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PMID:[Tomodensitometry: localizing value in hypertension of adrenal origin (author's transl)]. 49 67

To study whether the renin-angiotensin system is related to hyperuricemia in hypertension, the serum concentration of uric acid was determined in 96 patients with various types of hypertension and various degrees of plasma renin activity (PRA). In malignant hypertension, both PRA and the serum uric acid level were higher than in essential hypertension; but in primary aldosteronism or desoxycorticosterone-excess hypertension, they were lower than in the essential type. In renovascular hypertension, PRA was higher than in essential hypertension, but the serum uric acid levels were similar. There were no differences in PRA and serum uric acid concentration between Cushing's syndrome and essential hypertension. The serum uric acid level in high-renin essential hypertension was higher than in either the normal-renin or the low-renin type. There was a significant correlation between serum uric acid concentration and PRA in the basal state, and between the change in PRA and the change in serum uric acid induced by administration of furosemide. Apparently the close correlation between the renin-angiotensin system and the concentration of serum uric acid is related to changes in extracellular fluid volume, although an intrarenal effect of angiotensin II cannot be excluded.
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PMID:Serum uric acid and the renin-angiotensin system in hypertension. 65 66

Plasma 11-deoxycorticosterone levels were manyfold elevated in three adult patients with hypertension and elevated urinary excretion levels of 17-ketosteroids but without Cushing's syndrome. Dexamethasone therapy resulted in suppression of these steroids and in improvement of blood pressure in two of the patients. A partial adrenal 11beta-hydroxylase deficiency appears to best explain these findings.
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PMID:Deoxycorticosterone and 17-ketosteroids. Elevated levels in adult hypertensive patients. 66 Aug 29

A method for simultaneous measurement of 11-deoxycorticosterone (DOC), 18-hydroxy-11-deoxycorticosterone (18-OH-DOC) and aldosterone using 1.0-2.0 ml of plasma has been developed. The present method consists of extracting plasma with dichloromethane, separating the DOC, 18-OH-DOC, and aldosterone from other steroids on a Sephadex LH-20 column, and quantitating each steroid by radioimmunoassay. This method was demonstrated to be sensitive, accurate and precise. In 20 normal male subjects, the mean recumbent level of DOC was 9.1 +/- 3.1 ng/100 ml, on random diet, at 0800 h. The corresponding levels of 18-OH-DOC and aldosterone were 8.2 +/- 3.9 ng/100 ml, and 6.7 +/- 2.6 ng/100 ml, respectively. Plasma levels of these three steroids were measured in several types of adrenocortical disorders associated with hypertension and hypokalemia. Patients with Cushing's syndrome due to adrenocortical hyperplasia, and 17alpha-hydroxylase deficiency had elevated DOC and 18-OH-DOC levels, but showed normal or lower aldosterone levels. Hypersecretion of DOC and 18-OH-DOC may cause the symptoms of hypertension and hypokalemia. Patients with primary aldosteronism had elevated levels of DOC and 18-OH-DOC as well as aldosterone. The former two steroids may be hyperproduced as a precursor of aldosterone.
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PMID:Simultaneous determination of plasma 11-deoxycorticosterone, 18-hydroxy-11-deoxycorticosterone, and aldosterone in man. 66 34

Using RIA for determining the plasmatic renin activity in orthostatism according to the method of Fyhrquist we obtained in the control group of adult subjects nonsignificant variations in relation with sex and age, and in the group with Cushing's syndrome associated with arterial hypertension nonsignificantly increased values as against the controls. In pathologic pregnancy (toxemic pregnancy with arterial hypertension and edemas), the plasmatic renin (PR) activity was significantly higher ( less than 0.001) than in the group with physiologic pregnancy.
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PMID:Plasmatic level of angiotensin I in normal subjects of various ages, in Cushing's syndrome and in normal and pathologic pregnancy. 67 28

The blood pressure response to the angiotensin II analog 1-sar-8-ala-angiotensin II, or saralasin, was studied in five patients with clinical and laboratory evidence of Cushing's syndrome. Plasma renin activity, plasma renin substrate, and plasma renin concentration were measured in all five patients. The renin system and the response to saralasin were measured after furosemide administration. Plasma aldosterone was measured after infusion of 2 liters normal saline. All patients studied showed a hypotensive response to saralasin, the mean BP changing from 163/108 mm Hg to 130/85 mm Hg (P less than 0.02). There was a significant elevation of the plasma renin activity and plasma renin concentration in the patients compared to normal subjects, although plasma renin substrate was not significantly different from normal values. There was normal suppression of plasma aldosterone after the infusion of 0.9% saline. The findings indicate that the hypertension of these patients with Cushing's syndrome was mediated in large part by angiotensin II.
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PMID:Evidence for an angiotensinogenic mechanism of the hypertension of Cushing's syndrome. 75 14

The case of a young boy who had Cushing's syndrome and severe hypertension in association with metastatic adrenal carcinoma is described. Marked elevation of the mineralocorticoid 11-deoxycorticosterone was demonstrated in the plasma. 11-Deoxycortisol, 17alpha-hydroxyprogesterone, and urinary tetrahydro-11-deoxycortisol and pregnanetriol were also elevated. Aldosterone excretion was low. The data implicate defective 11beta hydroxylation and suggest that excessive 11-deoxycorticosterone production may have been responsible for the hypertension.
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PMID:Steroid profile in a case of adrenal carcinoma with severe hypertension. 86 97

Hypertension and hypokalemia occur in patients with Cushing's syndrome whereas aldosterone production is normal and plasma renin activity is usually normal or increased. A normal aldosterone level in the face of suppressed plasma renin activity is unusual and suggests excess mineralocorticoid hormone activity. Our patient, who had Cushing's syndrome due to adrenocortical adenoma, can be classified as having low renin hypertension (suppressed renin and normal aldosterone levels). The mineralocorticoid hormone in excess was deoxycorticosterone which suppressed renin. The aldosterone production was normal and was produced solely by the adenoma. Contralateral adrenal gland suppression of both the zona glomerulosa by deoxycorticosterone via renin, and of the fasciculata by cortisol via ACTH was demonstrated after removal of the adenoma. Normal adrenal function was gradually restored.
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PMID:Concurrent hypercortisolism and hypermineralocorticoidism. 87 Nov 29


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