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 review of some recent laboratory findings indicates definite disturbances in aldosterone metabolism and regulation in patients with mild essential hypertension: (a) a significant mean increase in plasma aldosterone concentration in patients with mild and stable essential hypertension, in contrast to the absence of any difference in patients with labile borderline essential hypertension when in a normotensive phase, compared with control subjects; and (b) a significant mean decrease in metabolic clearance rate of aldosterone, associated with a 12% decrease in hepatic blood flow and an increased binding of aldosterone to a transcortin-like plasma globulin. The secretion rate of 18-hydroxy-11-deoxycorticosterone is above the upper range of normal in 60% of patients with mild, uncomplicated essential hypertension. The incidence of low-renin hypertension, when age and race are taken into account, is much lower than previously assumed. Unless measurements are repeated over a long period, one or two low values of plasma renin cannot be considered a permanent marker indicating a special category of patients with essential hypertension. Tonin, a new enzyme discovered by Boucher, which forms angiotensin II directly from a plasma protein, from the tetradecapeptide substrate and from angiotensin I, is present in most tissues, but in highest concentration in the submaxillary gland. This enzyme is under the control of beta-adrenergic receptors.
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PMID:Aldosterone and renin in essential hypertension. 109 56

Patients with essential hypertension and hypertension complicated by coronary heart disease showed adrenal glucocorticoid activation along with reduced transcortin binding capacity (TBC). The addition of circulatory insufficiency (stage I and IIB) resulted in a decrease of the functional adrenal reserve and further diminution of TBC due to a reduction of protein binding sites concentration, and sometimes (stage IIB) also a decrease in the protein affinity of steroids. A correlation between TBC and plasma protein level was found. The absence of adrenal functional response to an abrupt drop in TBC is interpreted as a complete failure of the adaptation systems.
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PMID:[Functional activity of the adrenal glands and the hormone-protein interactions in patients with hypertension with a complicated course]. 337 89