title: Some metabolic, humoral and genetic aspects of arterial hypertension.
abstract: Our paper is discussing the presence and intensity of metabolic, humoral and haemodynamic abnormalities in mild middle-aged essential hypertensives (EH) and in hereditary predisposed still normotensive offspring from hypertensive families and their possible association with candidate genes changes. Four groups of subjects were compared (middle-aged normotensive controls (n = 21), corresponding patients with EH (n = 21), normotensive offspring from hypertensive (SH) (n = 56) and normotensive families (SN) (n = 56). Our results demonstrate that middle-aged patients with EH in our country have the same indices of hyperinsulinemia, impared glucose tolerance and insulin-sensitivity as previously described for other populations. They are accompanied by higher plasma concentrations of vasopressor substance like catecholamines, endothelin and lower levels of vasodepressor substances as ANP and kallikrein. The finding of similar, but quantitatively less expressed metabolic and humoral changes in SH but not in SN support the evidence for hereditary background of these abnormalities. The humoral and metabolic abnormalities may participate in BP elevation and in morphological and functional changes of left ventricle seen in SH (higher LV mass index, impaired diastolic filling). We did not prove an association between BP and polymorphism of ACE and angiotensinogen genes, however, our findings of association of DD genotype for ACE and M235 for angiotensinogen with higher insulinemia, plasma catecholamines and plasma renin activity evoke the hypothesis, whether the bearers of these genotypes, exposed for long-time to the higher concentrations of vascoactive substances, are not the subset of hereditary threatened subjects in whom clinically evident EH will manifest during their life.
authors.affiliation: 2nd Department of Medicine, Charles University Ist School of Medicine, Prague, Czech Republic.
authors.forename: K
authors.initials: K
authors.lastname: Horký
authors.forename: M
authors.initials: M
authors.lastname: Jáchymová
authors.forename: A
authors.initials: A
authors.lastname: Jindra
authors.forename: J
authors.initials: J
authors.lastname: Peleska
authors.forename: V
authors.initials: V
authors.lastname: Umnerová
authors.forename: S
authors.initials: S
authors.lastname: Heller
authors.forename: O
authors.initials: O
authors.lastname: Lisý
authors.forename: J
authors.initials: J
authors.lastname: Bultas
mesh_terms: D000328:Adult; D000808:Angiotensinogen / Q000235:genetics; D002096:C-Peptide / Q000097:blood; D004198:Disease Susceptibility; D004452:Echocardiography; D004837:Epinephrine / Q000097:blood / Q000235:genetics; D005838:Genotype; D006801:Humans; D006946:Hyperinsulinism / Q000150:complications; D006973:Hypertension / Q000000981:diagnostic imaging / Q000503:physiopathology*; D007610:Kallikreins / Q000652:urine; D008297:Male; D009638:Norepinephrine / Q000097:blood / Q000235:genetics; D007703:Peptidyl-Dipeptidase A / Q000235:genetics; D011110:Polymorphism, Genetic
chemical_list: D002096:C-Peptide; D000808:Angiotensinogen; D007703:Peptidyl-Dipeptidase A; D007610:Kallikreins; D009638:Norepinephrine; D004837:Epinephrine