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)

Urinary excretion of kallikrein has been studied in a patient with hypokalemic alkalosis, hyperplasia of the renal juxtaglomerular apparatus and hyperreninemia, secondary aldosteronism and resistance to the pressor effect of angiotensin II (Bartter's syndrome). Urinary kallikrein was found exceedingly high in several determination, whereas it was low in patients with essential hypertension and high in patients with primary aldosteronism. Urinary kallikrein decreased after spironolactone therapy. The rise of kallikrein excretion (which is not related to plasma renin) in this case is probably caused by a direct action of the chronic excess of plasma aldosterone; it could not be accounted for as secondary to natriuresis.
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PMID:Urinary kallikrein excretion in Bartter's syndrome. 99 21

Among the forms of endocrine hypertension, attention has recently been turned, apart from pheochromocytoma, to hypertensions caused by overproduction of mineralocorticoids. In this category are included, in addition to the classic Conn syndrome, aldosteronism associated with bilateral adrenal hypertrophy, dexamethasone-suppressible aldosteronism, and overproduction of mineralocorticoids (other than aldosterone) in the case of defects in the steroidogenesis enzyme system. In these cases, mineralocorticoid overproduction is accompanied by a low level of renin, by hypokalemic alkalosis. Secondary hyperaldosteronism, due to the stimulation of aldosterone secretion by increased activity of the renin-angiotension system, occurs during the malignant phase and in cases of renovascular hypertension. Estrogens, in cyclically secreted physiological quantities, have rather a protective effect on the origination of hypertension. At high dosages (as in contraceptives), estrogens can induce or aggravate hypertension in susceptible women by their effect on the activity of the renin-angiotensin-aldosterone system, notably by increasing the renin substrate. In the case of essential hypertension, deviations were found in the functioning of catecholamine storage granules in the sympathetic nerve endings. The renin-angiotensin-aldosterone system functions as an accelerating factor only in the advanced phase of essential hypertension, and the possibility of its participation in development of malignancy cannot be eliminated. A special group is comprised of essential hypertension with renin suppression, which is associated with a relatively high level of urinary excretion of dopamine as compared with noradrenalin. In renovascular hypertension, the renin-angiotensin-aldosterone system most often functions as an etiopathogenetic factor at the onset of the disease. In advanced stages, increased blood pressure levels must be considered to be attributable to other factors. Blood pressure regulati on and idiopathogenesis in hypertension cases are complex processes induced by the interaction of several different hemodynamic, nervous, and humoral factors. The study of humoral factors contributes to etiopathogenetic understanding and to the differential diagnosis of the various kinds of hypertension.
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PMID:[New data on hormone-dependent hypertension and their significance for the practice]. 434 13

The effects of 2 potassium-retaining diuretics on arterial pressure, intravascular volume, responses of the renin-angiotensin-aldosterone system, serum electrolytes, and renal function were compared by means of an 8-wk double-blind, crossover trial in 13 patients with "volume-dependent" essential hypertension. The fall in systolic, diastolic, and mean arterial pressures in the supine and erect positions (all p less than 0.005) induced by spironolactone was greater than that by triamterene. The pressure fall induced by spironolactone was also associated with a persistent contraction in plasma volume (p less than 0.05) and a secondary hyperaldosteronism that was not accompanied by hypokalemic alkalosis. The pressure fall induced by triamterene was not associated with reduced plasma volume, effect on plasma renin activity, or aldosterone excretion. Both drugs produced significant rises in blood urea nitrogen and creatinine levels that never exceeded normal limits.
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PMID:Spironolactone and triamterene in volume-dependent essential hypertension. 698 54

Severe low-renin hypertension has few known causes. Apparent mineralocorticoid excess (AME) is a genetic disorder that results in severe juvenile low-renin hypertension, hyporeninemia, hypoaldosteronemia, hypokalemic alkalosis, low birth weight, failure to thrive, poor growth, and in many cases nephrocalcinosis. In 1995, it was shown that mutations in the gene (HSD11B2) encoding the 11beta-hydroxysteroid dehydrogenase type 2 enzyme (11beta-HSD2) cause AME. Typical patients with AME have defective 11beta-HSD2 activity, as evidenced by an abnormal ratio of cortisol to cortisone metabolites and by an exceedingly diminished ability to convert [11-3H]cortisol to cortisone. Recently, we have studied an unusual patient with mild low-renin hypertension and a homozygous mutation in the HSD11B2 gene. The patient came from an inbred Mennonite family, and though the mutation identified her as a patient with AME, she did not demonstrate the typical features of AME. Biochemical analysis in this patient revealed a moderately elevated cortisol to cortisone metabolite ratio. The conversion of cortisol to cortisone was 58% compared with 0-6% in typical patients with AME whereas the normal conversion is 90-95%. Molecular analysis of the HSD11B2 gene of this patient showed a homozygous C-->T transition in the second nucleotide of codon 227, resulting in a substitution of proline with leucine (P227L). The parents and sibs were heterozygous for this mutation. In vitro expression studies showed an increase in the Km (300 nM) over normal (54 nM). Because approximately 40% of patients with essential hypertension demonstrate low renin, we suggest that such patients should undergo genetic analysis of the HSD11B2 gene.
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PMID:A genetic defect resulting in mild low-renin hypertension. 970 24