Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A simplified radioimmunoassay of urinary aldosterone is reported. Acid-hydrolyzed urine was extracted with dichloromethane and the extract assayed without further purification, Urinary aldosterone values in patients with Cushing's syndrome, low and normal-renin essential hypertension, congenital adrenal hyperplasia, and primary aldosteronism determined by this method agreed closely (r = 0.95, P less than 0.01) with values obtained using a standardized chromatographic method. This simplified assay represents a significant advance in out capabilitites for evaluating patients for abnormalities in aldosterone physiology.
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PMID:Urine aldosterone radioimmunoassay: validation of a method without chromatography. 127 May 82

The paper deals with the results of investigations of steroidogenesis in patients with ACTH-dependent Icenko-Cushing's disease (CD), congenital adrenal hyperplasia (CAH), and stromal hyperthecosis (SH). Along with the traditional methods of evaluating the activity of steroid-producing glands (diurnal variations of steroid hormones and their precursors in the peripheral blood, their mean daily concentrations), the authors used a simultaneous selective catheterization technique for adrenal and ovarian veins. No pronounced circadian rhythms were revealed in most of the steroids measured in patients with CD. A sharp rise in the mean daily serum 17-hydroxypregnenolone concentrations coupled with the steady-state 17-hydroxyprogesterone level is considered to reflect the activation of steroid biosynthesis via the delta 5-pathway. CD patients were demonstrated to exhibit great differences in the daily pattern of aldosterone secretion depending on the development of essential hypertension. CAH patients had high 17-hydroxypregnenolone and 17-hydroxyprogesterone levels. Like 17-hydroxyprogesterone, 17-hydroxypregnenolone may be used as a diagnostic marker of CAH. Hyperandrogenism in this disorder was largely due to enhanced adrenal production of testosterone and delta 5 androgens DHA and DHA-S. Unlike CAH, SH was not associated with excessive secretion of either DHA or DHA-S, but the ovaries of these patients released greater amounts of testosterone, which led to hyperandrogenism.
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PMID:[Steroidogenesis in patients with various adrenal and gonadal dysfunctions]. 762 95

The results of many studies performed on animals and humans strongly suggest that genetic factors lead to the development of hypertension (HT). Syndromes in which mutations in single genes are sufficient to result in large changes of blood pressure are rare. Nevertheless, it is anticipated that their understanding will lead to new insights into forms of hypertension occurring more often, including essential hypertension. At least 9 monogenic forms of HT including Liddle syndrome, type I familial hyperaldosteronism (GRA) and type II familial hyperladosteronism, Gordon syndrome, apparent mineralocorticoid excess syndrome (AME), hypertension associated with type E brachydactyly, glucocorticoid receptor mutations, type IV congenital adrenal hyperplasia (CAH) (11 beta-hydroxylase deficiency), and type V CAH (17 alpha-hydroxylase deficiency) have been described so far.
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PMID:[Monogenic hypertension]. 1505 25

The knowledge of the genetic bases of hypertension has improved over the last decade; this area of research has high priority due to the high incidence of hypertension and its impact on public health. Monogenetic mineralocorticoid hypertension syndromes are associated with suppressed plasma renin activity due to excessive activation of the mineralocorticoid pathway. We review the pathophysiology, phenotype, and method of diagnosis for familial hyperaldosteronism type I and type II, hypertensive forms of congenital adrenal hyperplasia, 11beta-hydroxysteroid dehydrogenase type 2 deficiency, Liddle's syndrome, an activating mutation of the MR, and glucocorticoid resistance. We also review some genes that could contribute to essential hypertension.
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PMID:Genetics of hypertensive syndrome. 1933 89