PP.21.22

Abstract

Objective: To evaluate whether usual antihypertensive drugs modify cardiac morphology in spontaneously hypertensive rats (SHR). We show that these drugs modify cardiac function in SHR in other study presented in this congress. Design and method: Male SHR 8 weeks age were randomly assigned to different antihypertensive oral treatment (n = 18/group) for 16 months: losartan 30 mg/kg (L), hydralazine 11 mg/kg (H), rosuvastatin 10 mg/kg (R), carvedilol 20 mg/kg (C) (n = 16), water (SHRw treatment control). Hypertension control group was comprised of 18 normotensive Wistar Kyoto rats (WKY). Histology: conventional light microscopy. Morphology: Image-Pro Plus 6.0 software. Morphometry: area of 237 ± 50 myocytes (transversal section, μm2), number of myocytes/mm2, number of capillaries/mm2 (N). Average oxygen diffusion distance (myocyte-to-capillary) was calculated (R, μm). Stereology: determination of the number of points by counting (Pp), estimation of volumetric density (Vv) for myocardium, interstitium and coronary capillaries as Vv (%) = [Pp /Ptotal] x 100. Statistics: Kruskal Wallis non parametric test, Dunn test for multiple comparisons (Graph Pad Prism, 5.0). Significance: p < 0.05. Results: Table 1 (on the following page) shows full morphometry data; (n) = number of cases, a p < 0.01 vs SHRw; b p < 0.05 vs SHRw; c p < 0.01 vs SHRw, C, H, R, WKY; d p < 0.05 vs R, H.Conclusions: Losartan treatment increased the number of capillaries and cardiomyocytes of normal size, reduced interstitial volume and myocyte-to-capillary distance in LV. Rosuvastatin treatment increased the number of capillaries in both ventricles. These findings and inhibition of LVH development with normalization of basal inotropism and beta adrenergic response as shown in other presentation in this Congress, point out that Losartan might be the most effective antihypertensive of those presently examined. It follows that activation of angiotensin II receptors might be a key step in LVH development with decline in beta adrenergic response in hypertension. The presence of LVH or cardiac failure was associated with expression of thioredoxins only in some cases suggesting that oxidative stress may not be determinant in LVH development.