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

Adenomas of the adrenal cortex which produce aldosterone (APA) are among the surgically correctible causes of hypertension accounting for 0.5 to 1.0% of all hypertensive etiologies. The adenomas have a 5:1 predilection for women and generally present with hypertension or profound hypokalemia. A low plasma renin activity completes the triad for primary hyperaldosteronism which could be caused by adrenocortical cancer, a neoplasm with an average diameter of 12 cm, or idiopathic hyperaldosteronism (IHA), a bilateral hyperplasia of the zona glomerulosa of the adrenal cortex which responds poorly to surgical resection. The adenomas are small (2 cm) but can be localized by imaging or selective venous sampling. Resection has a high success rate with minimal morbidity.
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PMID:Aldosterone-producing tumors (Conn's syndrome). 218 43

We describe four cases of primary hyperaldosteronism whose initial presentation was a moderate to severe hypertension. In three patients an adrenal adenoma was found; in another patient was due to unilateral adrenal hyperplasia. A good therapeutic response was achieved in all cases by unilateral adrenalectomy. The captopril test (Lyons version) proved useful to exclude essential hypertension and, may be, in distinguishing the new sub-types of primary hyperaldosteronism recently described. Indeed, only in the case of unilateral adrenal hyperplasia a fall in plasma aldosterone levels was observed. However, we feel that further investigation is needed to clarify this point.
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PMID:[Significance of the captopril test in the diagnosis of primary hyperaldosteronism --apropos of 4 clinical cases]. 220 22

Modern, views are presented on the pathogenesis of arterial hypertension in certain diseases of endocrine glands. In patients with phaeochromocytoma, virilizing tumours, acromegaly, in Cushing's disease, and in Conn's syndrome at the present state of knowledge it is not possible to formulate unequivocal conclusions concerning the effects of renin-angiotensin-aldosterone system on the mechanism of arterial hypertension development in these endocrinopathies.
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PMID:[The renin-angiotensin-aldosterone (RAA) system in endocrine diseases]. 225 31

A unique case of 17 alpha-hydroxylase deficiency with steroid-responsive primary hyperaldosteronism is reported. Initially the patient was misdiagnosed as testicular feminization for 16 years and was thought to have typical primary hyperaldosteronism for 5 years. However, careful detailed endocrine studies showed markedly elevated progesterone, deoxycorticosterone, and 18-hydroxycorticosterone values with low levels of 17-hydroxyprogesterone, 11-deoxycortisol, testosterone, and DHEA-Sulfate. In contrast to the suppressed aldosterone levels that are found in 17 alpha-hydroxylase deficiency, this patient's aldosterone levels were inappropriately elevated before and after ACTH stimulation. Use of glucocorticoid replacement resolved the patient's symptoms and completely corrected the hypokalemia and hypertension. In summary, recognition of 17 alpha-hydroxylase deficiency with steroid-responsive primary hyperaldosteronism is important because hypertension, hypokalemia, and symptoms respond to steroid replacement.
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PMID:17 alpha-hydroxylase deficiency masquerading as primary hyperaldosteronism. 226 76

Primary hyperaldosteronism (Conn's syndrome) rarely occurs during pregnancy. The concurrence of hypertension combined with hypokalemia and revealing subjective symptoms such as paresthesia, muscular weakness and lassitude can suggest this infrequent diagnosis. The diagnosis is confirmed on the one hand by chemical tests demonstrating an aldosterone level far above normal and clearly suppressed renin activity, and on the other hand through ultrasound for a morphological diagnosis. We consider causal surgical treatment with adrenalectomy as the therapy of choice during early pregnancy.
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PMID:[Primary aldosteronism in pregnancy]. 234 11

This report describes two adolescents with severe hypertension secondary to renal artery stenosis who had evidence of a hypokalemic metabolic alkalosis in their initial laboratory evaluation. Hypokalemic metabolic alkalosis is known to occur in approximately 16% of adults with renal artery stenosis but has not been well described in the pediatric literature. It is the result of excess aldosterone secretion stimulated by renal artery stenosis-mediated activation of the renin-angiotension system and by an increase in natriuresis from the contralateral, non-stenotic kidney. Although primary hyperaldosteronism must be considered in children with hypertension and hypokalemia, it is a rare disease in children. This report supports current recommendations that the initial focus of medical investigation in the severely hypertensive child should remain on the kidney.
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PMID:Renovascular hypertension presenting with hypokalemic metabolic alkalosis. 239 86

The acute blockade of the renin-angiotensin system has been made it possible to investigate its role in the maintenance of blood pressure and aldosterone secretion in normotensive and hypertensive subjects. The administration of saralasin or captopril and, in the near future, of renin inhibitors induces a fall in blood pressure that is variable from one subject to the other according to the sodium balance and the level of activation of the system. These blockers also decrease the angiotensin II-dependent aldosterone production and increase renin secretion according to the circulating level of angiotensin II and the functional state of adrenal and juxtaglomerular receptors. In practice the definition of an abnormal response to renin-angiotensin blockade is difficult to define precisely, but the hypotensive effect has been tentatively used for the diagnosis of renin-dependent hypertension, especially renovascular hypertension and primary hyperaldosteronism. In renal artery stenosis the most convincing results mainly concern the lateralization of an abnormal unilateral renin secretion, which is potentiated by an acute blockade of the renin-angiotensin system. The acute administration of converting enzyme inhibitor is also useful to detect the absence of decrease in plasma aldosterone, which is characteristic of a solitary tumor or of other anatomical and functional disorders of the adrenal glands.
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PMID:Acute inhibition of the renin-angiotensin system: interest and limits to detect surgically curable hypertension. 241 19

The role of vasopressin in human hypertension was examined in a series of studies. In patients with primary hyperaldosteronism and benign essential hypertension, circulating vasopressin was generally lower than in normotensive subjects. In contrast, plasma vasopressin was increased (p less than 0.001) in patients with malignant-phase hypertension. However, compared to infused vasopressin in normal subjects, when plasma levels of up to 120 pg/ml did not affect blood pressure, the increased levels found in malignant hypertension could not account for the hypertension. The possibility that there may be an increased pressor sensitivity to vasopressin in hypertension was examined by infusing the peptide into nine patients with essential hypertension. This showed a slight increase in sensitivity compared to normotensive subjects, but again this was insufficient to account for the discrepancy between the circulating level of vasopressin and the extent of the raised blood pressure in the hypertensive patients. The effect of chronically elevated levels of vasopressin was studied in a group of patients with the syndrome of inappropriate ADH excess as a consequence of bronchogenic carcinoma. In spite of having chronically elevated levels of vasopressin, these patients had normal blood pressures for their age and sex. Our results suggest that, although vasopressin is elevated in malignant hypertension, it does not contribute significantly to the raised blood pressure, and its increase is probably a consequence of volume shrinkage through renal salt and water loss.
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PMID:Vasopressin and hypertension in man. 243 62

Primary aldosteronism is an uncommon cause of hypertension but one of particular interest because of its distinctive pathophysiological mechanism of blood pressure elevation. Aldosterone has been associated with increased Na+,K+-adenosine triphosphatase (ATPase) activity, but there is controversy over which sodium transport parameters are responsible for this increase. We measured intracellular sodium, ouabain-sensitive and ouabain-insensitive sodium efflux, and the number of Na+,K+-ATPase sites of washed erythrocytes, as well as Na+-Li+ countertransport and the Li+-K+ cotransport rate constant of lithium-loaded red blood cells (RBCs) in six patients with primary aldosteronism and in 50 normal subjects. Ouabain-sensitive sodium efflux was significantly (p less than 0.001) higher for the primary aldosteronism patients than for normal subjects (1.85 +/- 0.29 vs 1.51 +/- 0.21 mmol/L RBC/hr) even though the intracellular sodium concentration (7.2 +/- 1.5 vs 6.7 +/- 1.9 mM) and the number of the Na+,K+-ATPase sites per RBC (331 +/- 52 vs 385 +/- 97) were not increased. The elevated sodium efflux appeared to be due to a significant (p less than 0.001) increase in the rate constant (1.60 +/- 0.12 x 10(-15) vs 1.28 +/- 0.15 x 10(-15) mmol/site/hr) of the ouabain-sensitive sodium efflux. The rate constant decreased significantly (p less than 0.01) after treatment.
Hypertension 1988 Feb
PMID:Sodium transport parameters in erythrocytes of patients with primary aldosteronism. 244 94

Atrial natriuretic peptide is a recently discovered cardiac hormone with natriuretic, vasodilatory and hypotensive activities. The role of this hormone in the pathophysiology of hypertension is of particular interest. In contrast to an earlier concept, a deficiency of the atrial peptide could not be found in animal models of hypertension or in patients. ANP plasma levels were elevated in SHR with accelerated hypertension, in salt-sensitive Dahl rats, in rats with DOCA-salt-hypertension and in animals with renovascular hypertension. Elevated ANP levels under these conditions can be explained by an expansion of the intravascular volume or by an elevated atrial wall stretch induced by the hypertension itself. In patients with primary hypertension, plasma levels of the peptide are raised in some patients and are normal in others. Plasma ANP levels correlate with age, blood pressure and signs of left ventricular hypertrophy. A negative correlation is described between ANP and renin. Measurement of plasma ANP levels does not allow a differentiation between primary and secondary forms of hypertension. Elevated ANP levels are also found in primary hyperaldosteronism and in renal failure. Stimulation of ANP secretion by physical exercise and dietary salt loading is maintained in hypertension. Infusion of 1-28-hANP leads to a reduction in systemic arterial pressure in normotensives and hypertensives. The natriuresis induced by exogenous ANP is more pronounced in hypertensives. Stimulation of endogenous ANP secretion does not prevent the rise in blood pressure possibly due to a reduction in ANP receptors in target tissues.
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PMID:[Atrial natriuretic peptide and its significance for arterial hypertension]. 253 Dec 53


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