title: Selective mineralocorticoid receptor blocker eplerenone reduces resistance artery stiffness in hypertensive patients.
abstract: Some antihypertensive agents may improve resistance artery remodeling in hypertensive patients whereas other agents may not, for similar blood pressure reduction. We questioned whether the selective mineralocorticoid receptor blocker eplerenone improves resistance artery remodeling in hypertensive patients versus the beta-blocker atenolol. Sixteen hypertensive patients were randomly assigned to double-blind daily treatment with eplerenone or atenolol. Resistance arteries from gluteal subcutaneous tissue were assessed on a pressurized myograph. After 1 year of treatment, systolic and diastolic blood pressures were similarly well controlled in both groups. Endothelial function did not change with treatment in either group. Media/lumen ratio and cross-sectional area were unchanged in either the atenolol or the eplerenone group. In atenolol-treated patients, the arterial wall became stiffer, whereas in the eplerenone-treated patients, it became less stiff and similar to that of a normotensive control group. The media collagen/elastin ratio was reduced only after eplerenone treatment. Circulating concentrations of osteopontin, monocyte chemoattractant protein-1, basic fibroblast growth factor, interleukin-8, and interleukin-10 were significantly reduced only by eplerenone. However, plasma interleukin-1 receptor a concentration was significantly reduced by both drugs. In conclusion, in hypertensive patients, blood pressure control for 1 year with atenolol was associated with increased wall stiffness of resistance arteries, whereas eplerenone treatment was associated with reduced stiffness, decreased collagen/elastin ratio, and a reduction in circulating inflammatory mediators. These data raise the possibility that eplerenone treatment of hypertensive patients when normalizing blood pressure could potentially be associated with better vascular protection and outcomes than the beta-blocker atenolol, which remains to be demonstrated.
authors.affiliation: Lady Davis Institute for Medical Research, Sir Mortimer B. Davis-Jewish General Hospital, McGill University, Montreal, Quebec, Canada.
authors.forename: Carmine
authors.initials: C
authors.lastname: Savoia
authors.forename: Rhian M
authors.initials: RM
authors.lastname: Touyz
authors.forename: Farhad
authors.initials: F
authors.lastname: Amiri
authors.forename: Ernesto L
authors.initials: EL
authors.lastname: Schiffrin
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000328:Adult; D001158:Arteries / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology*; D001262:Atenolol / Q000627:therapeutic use; D001794:Blood Pressure / Q000187:drug effects; D002081:Buttocks; D003094:Collagen / Q000378:metabolism; D003971:Diastole; D004311:Double-Blind Method; D004548:Elasticity / Q000187:drug effects; D004549:Elastin / Q000378:metabolism; D000077545:Eplerenone; D005260:Female; D006801:Humans; D006973:Hypertension / Q000188:drug therapy* / Q000503:physiopathology*; D018836:Inflammation Mediators / Q000097:blood; D008297:Male; D008875:Middle Aged; D000451:Mineralocorticoid Receptor Antagonists / Q000627:therapeutic use; D009213:Myography; D013148:Spironolactone / Q000031:analogs & derivatives* / Q000627:therapeutic use; D040521:Subcutaneous Tissue / Q000098:blood supply; D013599:Systole; D014655:Vascular Resistance / Q000187:drug effects*
chemical_list: D000319:Adrenergic beta-Antagonists; D018836:Inflammation Mediators; D000451:Mineralocorticoid Receptor Antagonists; D013148:Spironolactone; D001262:Atenolol; D000077545:Eplerenone; D003094:Collagen; D004549:Elastin