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  • Title: [Endothelin plasma levels in various stages and types of arterial hypertension].
    Author: Horký K, Nĕmecek K, Widimský J, Jáchymová M, Jindra A, Savlíková J, Peleska J, Umnerová V, Jarolím M.
    Journal: Cas Lek Cesk; 1994 Jun 27; 133(13):407-10. PubMed ID: 8062334.
    Abstract:
    BACKGROUND: It can be assumed that endothelin (ET) the hitherto most powerful known vasoconstricting agent participates in the regulation of BP. The objective of this investigation was to compare ET plasma concentrations in different stages and types of arterial hypertension and to assess its possible participation in a rise of the BP. METHODS AND RESULTS: The authors assessed plasma concentration of ET1,2, using the RIA method, in 27 normotensive controls, 30 normotensive subjects with a family-history of hypertension, 21 patients with mild essential hypertension (EH), eight severe cases of EH and 27 patients with chronic renal failure who were in a regular dialyzation programe, incl. 13 treated on account of hypertension; in 14 the BP was within the normal range. The ET examination was supplemented by RIA assessment of the plasma renin activity (PRA). The authors recorded significantly higher ET concentrations as compared with controls (14.0 +/- 0.9 fmol/ml) in normotensive subjects from hypertensive families (18.1 +/- 1.2 fmol/ml), severe EH (26.1 +/- 3.2 fmol/l). Hypertensive patients with chronic renal failure (CHRS) had also higher ET levels (26.5 +/- 2.8 fmol/l). Patients with mild hypertension did not differ as regards ET concentrations (13.8 +/- 2.4 fmol/ml from controls. A significant increase of PRA was recorded in severe EH (3.4 +/- 1.2 ng/ml/hour) and in CHRS with hypertension (5.2 +/- 1.3 ng/ml/hour) as well as without hypertension (5.6 +/- 1.5 ng/ml/hour). CONCLUSIONS: The author's findings of elevated ET1,2 concentrations in subjects with a family disposition to hypertension, in advanced EH in renal hypertension and in CHRS support the assumption that ET can participate in the initial stages in the development and later in the progression of arterial hypertension either directly or by potentiating other pressor agents, e.g. higher activities of the renin-angiotensin system.
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