Effect of enalapril (E) or furosemide/dihydralazine (F/D) treatment from week 8–12 in sham-op and SNX on intramyocardial arterioles and capillaries.

<p>Mean ± standard deviation.</p><p>a) p<0.05 vs. corresponding SHAM.</p><p>b) p<0.05 vs. SNX 8 wks.</p><p>c) p<0.05 vs. SNX 12 wks.</p><p>d) p<0.05 vs. SNX+E.</p

Effect of treatment with the ACE-I enalapril or furosemide/dihydralazine on systolic blood pressure (A) and myocardial interstitial fibrosis (B).

<p><b>A.</b> Enalapril (E) and furosemide/dihydralazine (F/D) treatment lowered systolic blood pressure (bp) in sham and SNX to the same extent. Two weeks after SNX systolic bp was not significantly different between the groups. From week 5 onward bp was significantly higher (p<0.01) in untreated SNX than in untreated sham. At week 7 bp was highest in the SNX+F/D group. Treatment with E and F/D significantly and comparably lowered bp in SNX and sham compared to untreated animals. Mean of systolic blood pressure measurements at weeks 2, 5, 7, 9 and 11 using tail plethysmography in conscious rats that were acquainted to the measuring conditions. *: p<0.01 compared to all other groups. +: p<0.05 compared to all other groups. <b>B.</b> The increase in myocardial interstitial tissue (%) in untreated SNX at week 12 is completely prevented by enalapril, but not by furosemide/dihydralazine treatment. *: p<0.05 vs SNX 12 weeks. +: p<0.05 vs corresponding sham.</p

Myocardial fibrosis in untreated sham operated animals (A), sham+enalapril (B), untreated SNX 12 weeks (C) and SNX + enalapril (D).

<p>Note increased myocardial fibrous tissue content (depicted in red) in untreated SNX at 12 weeks (C) compared to untreated and treated sham (A,B). Complete regression of interstitial fibrosis is seen at 12 weeks after 4 weeks treatment with enalapril (D).Sirius red stain, magnification x 400.</p

Effect of treatment with the ACE-I enalapril or furosemide/dihydralazine on cardiac mRNA expression of TGF-β (A), TIMP-1 (B) and TIMP-2 (B).

<p>Increased TGF-β mRNA expression in untreated SNX was lowered by both antihypertensive treatments. Cardiac TIMP-1 gene expression was also significantly higher in untreated SNX 12 weeks than in sham and SNX 8 weeks; RAS blockade by ACE-I and alternative antihypertensive treatment both lowered cardiac TIMP-1 gene expression in SNX animals. The same tendency was seen for TIMP-2 mRNA expression. The data are provided as box plots of the ΔCT analysis. ° indicate outlyers.</p

Experimental protocol (A) and left ventricular weight (B).

<p>A. Experimental protocol. B. Effect of treatment with the ACE-I enalapril or furosemide/dihydralazine on left ventricular weight (g). The increase in left ventricular weight (g) in untreated SNX at week 12 is completely prevented by enalapril, not by furosemide/dihydralazine treatment.</p

Animal data: Effect of treatment with enalapril (E) or furosemide/dihydralazine (F/D) from week 8–12 in sham-op and SNX rats, respectively.

<p>mean ± standard deviation, ¹ weight after perfusion fixation.</p><p>a) p<0.05 vs. corresponding SHAM.</p><p>b) p<0.05 vs. SNX 8 wks.</p><p>c) p<0.05 vs. SNX 12 wks.</p><p>d) p<0.05 vs. SNX+E.</p

Effect of enalapril (E) or furosemide/dihydralazine (F/D) treatment from week 8–12 in sham-op and SNX on the aortic wall.

<p>Mean ± standard deviation.</p><p>a) p<0.05 vs. corresponding SHAM.</p><p>b) p<0.05 vs. SNX 8 wks.</p><p>c) p<0.05 vs. SNX 12 wks.</p><p>d) p<0.05 vs. SNX+E.</p

Effect of treatment with the ACE-I enalapril (E) on aortic wall thickness and aortic remodelling in sham (A,B) and SNX rats (C,D).

<p>The increase in aortic wall thickness in untreated SNX (C) compared to untreated and E-treated sham (A,B) reversed by antihypertensive treatment with enalapril (D).</p