title: Aldosterone receptor inhibition alters the viscoelastic biomechanical behavior of the aortic wall.
abstract: Dynamic mechanical disturbances in the aortic wall may lead to progressive aortic dilation and possibly aneurysmal formation. Here, we investigated the previously unexplored effects of aldosterone inhibition on aortic wall viscoelastic properties in hyperlipidemic rabbits. Thirty-six New Zealand male rabbits, fed a standard diet for four weeks, were separated into three groups: control (C; n = 10), standard diet; eplerenone (A; n = 12), hyperlipidemic diet plus 100 mg/kg/d eplerenone (last 4 weeks); and vehicle (V; n = 14), hyperlipidemic diet (no eplerenone). After eight weeks, animals were sacrificed and rectangular strips from the aortic wall, cut in radial and axial orientations, were prepared. Fresh, saline-wetted strips at 37 degrees C were subjected to cyclic sinusoidal elongation from zero to 20% of the resting length at a frequency of 1 Hz. The dynamic biomechanical viscoelastic characteristics, 'elastin phase' low modulus (E(L)), 'collagen phase' high modulus (E(H)) and dissipated-energy index, were determined. Aortic tissue preparations were also examined histologically. Eplerenone increased aldosterone concentrations but did not affect blood pressure, cholesterol or potassium concentrations. There was a significant reduction of E(H) (from 3.40 to 1.80 MPa; P < 0.01) and E(L) (from 0.46 to 0.27 MPa; P < 0.05) in group A in the radial direction compared with group C. In the axial direction E(L) significantly increased in group A compared with group V (from 0.42 to 1.11 MPa; P < 0.01). Energy dissipation was not significantly different among groups, although there was a trend toward higher values in group A for both directions. Histological assessments revealed no significant differences in collagen or elastic fibers among groups. In conclusion, aldosterone receptor inhibition altered the viscoelastic properties of the aortic wall in hyperlipidemic rabbits without detectable microscopic changes in elastic or collagen fibers, an effect that progressively might predispose to dilation and/or aneurysmal formation.
authors.affiliation: Cardiology Department, University of Patras, Greece.
authors.forename: Spyridon I
authors.initials: SI
authors.lastname: Gkizas
authors.forename: Efstratios
authors.initials: E
authors.lastname: Apostolakis
authors.forename: Eirini
authors.initials: E
authors.lastname: Pagoulatou
authors.forename: Dimostenis
authors.initials: D
authors.lastname: Mavrilas
authors.forename: Dionysios J
authors.initials: DJ
authors.lastname: Papachristou
authors.forename: Efstratios
authors.initials: E
authors.lastname: Koletsis
authors.forename: Apostolos
authors.initials: A
authors.lastname: Papalois
authors.forename: Helen
authors.initials: H
authors.lastname: Papadaki
authors.forename: Dimitrios
authors.initials: D
authors.lastname: Alexopoulos
mesh_terms: D000450:Aldosterone; D000818:Animals; D001011:Aorta / Q000473:pathology*; D001696:Biomechanical Phenomena; D001794:Blood Pressure; D018450:Disease Progression; D004548:Elasticity; D000077545:Eplerenone; D006949:Hyperlipidemias / Q000188:drug therapy; D008297:Male; D000451:Mineralocorticoid Receptor Antagonists / Q000494:pharmacology; D011817:Rabbits; D013148:Spironolactone / Q000031:analogs & derivatives / Q000494:pharmacology; D014783:Viscosity
chemical_list: D000451:Mineralocorticoid Receptor Antagonists; D013148:Spironolactone; D000450:Aldosterone; D000077545:Eplerenone