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

Primary aldosteronism and renovascular hypertension are two different diseases in which renin determinations are necessary for establishment of diagnosis or therapeutic procedure. Low renin values which are not stimulated by acute stimuli combined with elevated plasma aldosterone concentrations confirm the diagnosis of primary aldosteronism. When in a patient with proven renal artery stenosis a significant difference in renal venous renin activity is observed between the two kidneys, a connection between hypertension and renal artery stenosis is likely when in addition the renin secretion of the unaffected kidney is suppressed. A favourable outcome for surgery can be predicted when the individual clinical picture in such a case is also considered. A similar view also holds for the connection between hypertension and unilateral small kidney not due to renal artery stenosis. In essential hypertension the plasma renin level makes it possible to a certain extent to predict whether a patient will benefit from diuretics or from beta-blocking agents. Despite this experience, however, renin determinations are not indicated in every case of essential hypertension. It has not been proven that the prognosis of this disease is improved by renin oriented monotherapy rather than by effective treatment with other antihypertensive agents.
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PMID:[The value of renin determination in the diagnosis of hypertension]. 0 81

A very high cortisol production rate (CPR) with elevated plasma ACTH was found in a hypertensive, hypokalemic, but otherwise healthy male patient. There were no symptoms or signs of Cushing's syndrome. The hypercortisolism appeared to be of the pituitary dependent type. During the follow-up of 36 months, no changes in outward appearance occurred, notwithstanding persistent hypercortisolism. The possibility of either Conn's syndrome or of an enzymatic defect in steroidogenesis could be ruled out. One of the three children (a healthy boy of 20 years) also showed hypertension and hypercortisolism. A possibly genetically determined hyposensitivity to the glucocorticoid action of cortisol is postulated.
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PMID:Spontaneous hypercortisolism without Cushing's syndrome. 18 77

Primary hyperaldosteronism usually causes moderate hypertension. It is rare to note as in our two patients intermittent attacks of paroxysmal hypertension. The diagnosis of aldosteronism will be suspected on the finding of persistent hypokalemia with acidosis. It will be confirmed by laboratory examinations severe fall in plasma renin activity and rise in aldosterone in the adrenal veins. To determine the affected side, one may carry out adrenal phlebography which is a difficult technic, and/or a scan using iodine cholesterol which is benign and precise. Surgery with removal of the adenomatous hyperplasia in one case and of an adenoma in the other, gave one very good result.
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PMID:[Primary hyperaldosteronism with paroxysmal arterial hypertension. Apropos of 2 operated cases]. 20 43

The authors discuss the radiological signs in 18 patients with an adrenal tumour. 7 of them had a Cushing's syndrome, 10 others a phaechromocytoma and the last had primary hyperaldosteronism. The diagnosis was made from the history, the clinical picture, hormone estimations and pharmacodynamic tests, whilts in the majority of cases the tumour was localised by radiodiagnosis. In all cases, there was hypertension, permanent in tumours of the adrenal cortex, paroxysmal or permanent in the cases of pheochromocytomas. We emphasise the importance of retro-pneumoperitoneum, as the radiological investigation of choice, in the localisation of adrenal tumours, especially pheochromocytomas, and in Cushing's syndrome. In cases of pheochromocytoma, one should follow carefully the blood pressure, during special radiological investigations, in view of the danger of a sudden rise or fall in blood pressure, the first is treated with phentolamine, the second with noradrenaline solution. Finally, a scan using I 131 19-iodocholesterol may be valuable in diagnosis and localisation of adrenal tumours; it has in particular given very encouraging results in the differential diagnosis of adrenal tumours with the clinical presentation of Cushing's disease.
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PMID:[Radiological signs of tumours of the adrenal glands (author's transl)]. 21 64

Rectal potential difference (pd) is directly related to the plasma aldosterone concentration, and rises when aldosterone is stimulated by sodium deprivation. However, when the measurement of rectal pd was tested at a screening test for hyperaldosteronism in 19 hypertensive subjects, four of the eight with primary hyperaldosteronism had a normal pd and four of the eight without aldosterone excess had an abnormally raised potential difference. The technique cannot therefore be recommended as a routine screening test for hyperaldosteronism. No relationship was found between rectal pd and hypertension associated with excess of deoxycorticosterone. Rectal pd rises in response to the mineralocorticoid-like agent carbenoxolone.
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PMID:Rectal potential difference in the diagnosis of aldosterone excess. 23 2

The angiotensin II antagonist 1-sar-8-ala-angiotensin II (saralasin) was infused in forty-six patients with hypertension of various aetiology (essential, renal arterial or parenchymal disease, primary hyperaldosteronism), before and/or during sodium volume depletion obtained by chlorthalidone and low sodium diet. When saralasin was infused in twenty-five patients ingesting 130 mmol of sodium per day, including patients with proven renovascular hypertension, the changes in mean arterial pressure and ranged from +10 to -7 mmHg (mean: +0.20 mmHg) and were not related to the plasma renin concentration (PRC) (r = -0.11). During sodium volume depletion, saralasin induced changes in mean arterial pressure, ranging from +21 to -76 mmHg, which were closely related to log PRC (n = 32; r = -0.87). Combined sodium depletion and antagonism of angiotensin II 'normalized' mean arterial pressure (less than or equal to 100 mmHg) in twenty-one of the thirty-two patients, while pressure remained between 106 and 147 mmHg in eleven 'poor' responders, so that pressor mechanisms other than sodium volume and angiotensin must be responsible for the remaining elevation of pressure in these patients. The study indicates that arterial pressure is not dependent on the immediate pressor effects of angiotensin II in sodium replete patients, and in sodium deplete subjects whose PRC remains low, while it is at least partly angiotensin II dependent during sodium volume depletion in the others. The results cast doubts on the clinical usefulness of saralasin in the investigation of patients with hypertension, when studied in the conditions of the present study.
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PMID:Effects of the angiotensin II antagonist 1-sar-8-ala-angiotensin II in hypertension in man. 41 68

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

24 h-urine excretion of aldosterone-18-glucuronide was determined with and without preceding paper chromatography in patients with essential hypertension (n = 50). Radioimmunoassay was performed with a highly specific antibody against aldosterone. Urine specimens determined without chromatography gave significantly higher values than aliquots which were estimated at the same time with chromatography. A highly significant correlation was found between the two methods (r = 0.91, p less than 0.0001). Without chromatography, mean over estimation in samples with concentrations in the low and middle range was on average 32 and 24% respectively, whereas aldosterone concentrations in the upper range showed a 14% over estimation. The RIA procedure for aldosterone without chromatography as here described is suitable for hypertension screening programmes to exclude known forms of primary hyperaldosteronism in which elevated aldosterone excretion rates have to be differentiated from values lying within the normal range.
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PMID:Aldosterone 18-glucuronide excretion determined with and without chromatography in human hypertensives. 51 5

Personal experience in the management of three cases of primary hyperaldosteronism, in which a cure was obtained by surgical removal of an adrenocortical adenoma, is was used in the elaboration of a diagnostic procedure requiring hospitalisation for 12 days. During 6 days, the patient is kept on a diet containing 100 mEq Na and K, and blood potassium values are repeatedly determined. Other causes of hypertension are ruled out. On the 6th day, baselines for blood renin and urinary aldosterone are calculated. Next, a hyposodic diet is given for 4 days, and a diuretic is administered on the last of these days, after which renin is determined "in response to stimulation". Lastly, two days of i.v. NaCl loading are followed by the determination of urinary aldosterone "during inhibition". If the picture is positive for hyperaldosteronism, the patient is discharged and followed during treatment with spironolactone, and eventually subjected to renal and adrenal arteriography to determine the site of the adenoma. Division of the procedure into increasingly complex steps enables the examination to be halted at any point when evidence in support of the suspected diagnosis fails to appear. This feature, coupled with the simplicity of the procedures adopted, enables all young subjects admitted for unexplained hypertension to be screened for hyperaldosteronism, with the assurance of obtaining certain diagnosis without an excessively long stay in hospital.
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PMID:[Primary hyperaldosteronism. Diagnostic procedure useful in hospital routine]. 63 79

Factor VIII complex was studied in patients presenting arterial hypertension. Visceral involvement was quantified using a clinical index calculated from ocular fundus, renal function and left ventricular hypertrophy data. A significant correlation was found between the mean arterial pressure, the visceral involvement and the level of complex VIII. Nevertheless, other data obtained in different patients (Conn's disease) suggest that the visceral involvement (and not the mean arterial pressure) is the main determining factor in the increase of factor VIII complex.
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PMID:Increased level of factor VIII complex in severe arterial hypertension. 72 Sep 55


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