Plasma Endothelin-1 Levels in Obese Hypertensive and Normotensive Men

Abstract

Plasma endothelin-1 (ET-1) levels were studied in 15 obese hypertensive (mean age 48.5 +/- 3.9 years) and 15 obese normotensive men (mean age 49.5 +/- 3.6 years) before and after weight loss due to an 800 kcal/day diet lasting 12 weeks. Circulating peptide concentrations were also assessed in nonobese hypertensive (n = 11) and normotensive men (n = 12). Baseline plasma ET-1 levels were similar in obese hypertensive (0.87 +/- 0.22 pg/ml) and obese normotensive men (0.91 +/- 0.30 pg/ml). In seven obese hypertensive men, caloric restriction normalized blood pressure levels (systolic: from 166.6 +/- 8.1 to 145.0 +/- 6.3 mmHg, P < 0.0001; diastolic: from 106.6 +/- 5.1 to 89.1 +/- 2.0 mmHg, P < 0.0001) and decreased body mass index (BMI) (from 33.4 +/- 1.6 to 29.6 +/- 2.1 kg/m2, P < 0.002) and plasma ET-1 levels (from 0.93 +/- 0.21 to 0.64 +/- 0.26 pg/ml, P < 0.05). In the remaining obese hypertensive men (n = 8), blood pressure levels were not normalized by caloric restriction despite a significant decrease of BMI and plasma ET-1 levels (from 0.83 +/- 0.23 to 0.60 +/- 0.16 pg/ml, P < 0.04). Weight loss also significantly decreased BMI and ET-1 (from 0.91 +/- 0.30 to 0.65 +/- 0.19 pg/ml, P < 0.01) in obese normotensive men. Baseline ET-1 and fasting insulin levels were significantly correlated in obese hypertensive (r = 0.518, P < 0.05) and obese normotensive men (r = 0.535, P < 0.04).(ABSTRACT TRUNCATED AT 250 WORDS)

Mechanisms of endothelial dysfunction in the metabolic syndrome

“…Although in the normal physiologic state, insulin stimulates NO synthesis and enhances NO-mediated vasodilatation, this action is blunted or reversed in the IR state [28,29]. Although the precise mechanism by which IR and hyperinsulinemia produces ED remains to be elucidated, it has been suggested that, in addition to the decreased synthesis and responsiveness of NO, IR is associated with increased production of endothelin-1, which may not only cause vasoconstriction, but probably also plays an important role in the development of hypertension frequently seen in patients with MS and DM [28][29][30].…”

Insulin Action in the Vasculature: Physiology and Pathophysiology

“…Elevated circulating levels of ET-1 have been reported in most [55, 56, 57, 58, 59, 60, 61]but not all [62, 63]studies of human insulin resistance. The ET-1 elevation has been reported to be proportional to the hyperinsulinemia [64, 65, 66], and a dietary weight loss can reduce both serum insulin and ET-1 concentrations [67]. Furthermore, acute endogenous and exogenous elevations in circulating insulin levels in normal controls and in insulin-resistant subjects have been shown to acutely elevate circulating ET-1 [56, 68, 69], although again dissenting findings exist [70, 71, 72].…”

Adipositas und Hypertonie

“…Eine verän-derte Kontraktilität der Gefäße, insbesondere gegen vasokonstriktorische Faktoren, ist infolge veränderter intrazellulärer Elektrolytkonzentrationen postuliert worden. Dementsprechend ist interessanterweise gefunden worden [10], daß die Plasmaspiegel des Vasokonstriktors Endothelin-1 bei Adipositas erhöht sind und daß die periphere Gefäßresistenz bei adiopösen Probanden vermindert ist. Ferner ist gezeigt worden, daß die wahrscheinlich Endothel-vermittelte Stickstoffoxid-abhän-gige vasodilatatorische Wirkung von Insulin [2] bei adipösen Probanden deutlich vermindert bzw.…”