title: Effects of eprosartan versus hydrochlorothiazide on markers of vascular oxidation and inflammation and blood pressure (renin-angiotensin system antagonists, oxidation, and inflammation).
abstract: Antagonists of the renin-angiotensin system, such as angiotensin type 1 (AT(1)) receptor inhibitors and angiotensin-converting enzyme inhibitors, are becoming increasingly popular agents in treating patients with systemic hypertension and minimizing organ damage. In the present study, we compared the effects of eprosartan, an AT(1) receptor inhibitor, with the diuretic hydrochlorothiazide in a group of newly diagnosed hypertensive patients with multiple risk factors for atherosclerosis. The subjects were monitored and tested at 0 and 4 weeks to determine their individual effects on vascular and inflammatory markers. Although blood pressure reduction was comparable between the 2 agents, there were notable differences in their effects on markers of inflammation and oxidation. We observed a 28% reduction in neutrophil superoxide anion generating capacity, a 34% reduction in soluble monocyte chemotactic protein-1, and a 35% reduction in soluble vascular cell adhesion molecule with eprosartan therapy (all p <0.05 from the start of therapy). In addition, eprosartan showed further benefit in its ability to increase low-density lipoprotein oxidation lag time, suggesting an increased resistance to oxidation and/or modification of low-density lipoprotein. Although hydrochlorothiazide was effective in blood pressure reduction, there were no significant changes in any of the above parameters after 4 weeks of treatment. These findings suggest that eprosartan, an AT(1) receptor inhibitor, effectively reduces systemic blood pressure and, compared with hydrochlorothiazide, suggests additional benefits in the vasculature by inhibiting mechanisms of inflammation and oxidation.
authors.affiliation: Emory University School of Medicine, Division of Cardiology, Atlanta, Georgia 30303, USA.
authors.forename: Syed T
authors.initials: ST
authors.lastname: Rahman
authors.forename: Wright B
authors.initials: WB
authors.lastname: Lauten
authors.forename: Qamar A
authors.initials: QA
authors.lastname: Khan
authors.forename: Sushant
authors.initials: S
authors.lastname: Navalkar
authors.forename: Sampath
authors.initials: S
authors.lastname: Parthasarathy
authors.forename: Bobby V
authors.initials: BV
authors.lastname: Khan
mesh_terms: D000179:Acrylates / Q000627:therapeutic use*; D000328:Adult; D057911:Angiotensin Receptor Antagonists; D000959:Antihypertensive Agents / Q000627:therapeutic use*; D001794:Blood Pressure / Q000187:drug effects*; D018932:Chemokine CCL2 / Q000235:genetics; D004305:Dose-Response Relationship, Drug; D005260:Female; D005786:Gene Expression Regulation / Q000187:drug effects; D006801:Humans; D006852:Hydrochlorothiazide / Q000627:therapeutic use*; D006973:Hypertension / Q000150:complications / Q000188:drug therapy; D007093:Imidazoles / Q000627:therapeutic use*; D007249:Inflammation / Q000150:complications / Q000188:drug therapy*; D008077:Lipoproteins, LDL / Q000187:drug effects; D008297:Male; D008875:Middle Aged; D009131:Muscle, Smooth, Vascular / Q000187:drug effects; D010084:Oxidation-Reduction / Q000187:drug effects*; D011945:Receptors, Angiotensin / Q000627:therapeutic use*; D012084:Renin-Angiotensin System / Q000187:drug effects*; D013876:Thiophenes; D016896:Treatment Outcome; D019010:Vascular Cell Adhesion Molecule-1 / Q000187:drug effects
chemical_list: D000179:Acrylates; D057911:Angiotensin Receptor Antagonists; D000959:Antihypertensive Agents; D018932:Chemokine CCL2; D007093:Imidazoles; D008077:Lipoproteins, LDL; D011945:Receptors, Angiotensin; D013876:Thiophenes; D019010:Vascular Cell Adhesion Molecule-1; D006852:Hydrochlorothiazide; C068373:eprosartan