Key result
BAY 41-2272 cotreatment abolished L-NAME-induced hypertension in rats (112 vs 173 mm Hg; P<0.01) and prevented cardiac hypertrophy and increased fibrosis areas.
Why the study?
Does BAY 41-2272 prevent hypertension and cardiac abnormalities in rats treated with chronic L-NAME?
Does BAY 41-2272 prevent hypertension and cardiac abnormalities in rats treated with chronic L-NAME?
Absolute Event Rate: 112% vs 173%
p-value: p=<0.01
BAY 41-2272, an sGC stimulator, prevents hypertension, cardiac hypertrophy, and fibrosis induced by NO synthase inhibition in a rat model.
Hypothesis-generating in L-NAME rat model; human trials required before clinical consideration.
This study evaluated the effects of BAY 41-2272 (BAY), a specific activator of sGC NO-independent action on changes of mean arterial blood pressure, heart and left ventricle weight indexes, cardiomyocyte hypertrophy (Vv) and fibrosis area induced by chronic N-nitro-L-arginine methyl ester (L-NAME) treatment in rats. The animals were divided into (a) control group, (b) L-NAME group, (c) L-NAME+BAY group, and (d) BAY group. Eight weeks of L-NAME treatment caused a significant increase in mean arterial blood pressure when compared with untreated rats (173 +/- 11.1 and 109 +/- 5.0 mm Hg, respectively; P < 0.01). L-NAME + BAY cotreatment abolished the L-NAME-induced hypertension (112 +/- 5.1 mm Hg; P < 0.01). Significant increases in heart and left ventricle weight indexes and in Vv were observed in the L-NAME-treated animals compared with control group, and concomitant treatment with BAY significantly attenuated this hypertrophic effect. Treatment with L-NAME presented several areas of repairing fibrosis in left ventricles, and this effect was also abolished by BAY cotreatment. Our results demonstrate that BAY 41-2272 inhibits hypertension and prevents heart abnormalities (cardiac hypertrophy and increased fibrosis areas) induced by NO synthase inhibition.
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Zanfolin et al. (2006) studied Hypertension and cardiac hypertrophy. BAY 41-2272 vs. L-NAME alone was evaluated on Mean arterial blood pressure (p=<0.01). BAY 41-2272 cotreatment abolished L-NAME-induced hypertension in rats (112 vs 173 mm Hg; P<0.01) and prevented cardiac hypertrophy and increased fibrosis areas.
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