title: [Possibilities of using indices of vascular wall function as markers of negative metabolic effects of treatment with thiazide diuretics in patients with essential hypertension].
abstract: To evaluate the influence of antihypertensive and metabolic effects of thiazide diuretics on vascular endothelial function and coronary risk (CR) in patients with essential hypertension (EH). Materials and methods. The study included 50 EH patients treated with indapamide retard (n = 25) or hydrochlorothiazide (n=25) during 12 weeks. Changes in blood pressure, blood lipid and glucose levels, Framingham algorithm-calculated coronary risk (CR), the brachial response to endothelium-dependent and endothelium-independent stimuli, studied by high-resolution ultrasound, were evaluated. Results. Indapamide retard (1.5 mg/day) and hydrochlorothiazide (25 mg/day) showed the similar antihypertensive effect. Indapamide retard was metabolically neutral whereas hydrochlorothiazide increased the blood levels of triglycerides and glucose by 15.3% (p < 0.05) and 12.2% (p < 0.05), respectively. The calculated CR decreased by 21.3% (p < 0.01) on indapamide retard treatment and practically unchanged on hydrochlorothiazide. There were significant group differences in the effects of the drugs on endothelium-dependent vasodilatation. The latter tended to improve by indapamide retard (+8.9%; p = 0.10) and to significantly worse by hydrochlorothiazide (-17.0%; p < 0.05). Hydrochlorothiazide-induced changes in total cholesterol, triglycerides, and low-density lipoprotein cholesterol were directly related to calculated CR changes (r = 0.69, r = 0.58, and r = 0.57, respectively; p < 0.01) and the changes in blood glucose levels were inversely related to those in vascular endothelial function (r = -0.52; p < 0.01). Such relations were not observed on indapamide retard. Conclusion. The negative metabolic effects of hydrochlorothiazide induce negative changes in vascular endothelial function just at early stages of therapy. These changes may be used as a predictor of a coronary risk during thiazide diuretic treatment in patients with EH.
authors.forename: A A
authors.initials: AA
authors.lastname: Semenkin
mesh_terms: D000328:Adult; D000368:Aged; D000959:Antihypertensive Agents / Q000008:administration & dosage / Q000009:adverse effects* / Q000627:therapeutic use; D001794:Blood Pressure / Q000187:drug effects; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology; D005260:Female; D006801:Humans; D006852:Hydrochlorothiazide / Q000008:administration & dosage / Q000009:adverse effects / Q000627:therapeutic use; D006973:Hypertension / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D007190:Indapamide / Q000008:administration & dosage / Q000009:adverse effects / Q000627:therapeutic use; D050356:Lipid Metabolism / Q000187:drug effects*; D008297:Male; D008875:Middle Aged; D049993:Sodium Chloride Symporter Inhibitors / Q000008:administration & dosage / Q000009:adverse effects* / Q000627:therapeutic use; D016896:Treatment Outcome; D014664:Vasodilation / Q000187:drug effects*
chemical_list: D000959:Antihypertensive Agents; D049993:Sodium Chloride Symporter Inhibitors; D006852:Hydrochlorothiazide; D007190:Indapamide