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In contrast, fasudil treatment markedly increased the heart weights and heart index (heart [http://www.selleckchem.com/products/gsk2656157.html GSK2656157 mw] weight/body weight) compared to the control group (Table 1). In aortic rings, the cumulative concentration�Cresponse to NE (10?9�C10?5?M) was markedly decreased in the l-NAME induced hypertensive rats compared to the control rats (P[http://en.wikipedia.org/wiki/Oxygenase Oxygenase] (P[http://www.selleckchem.com/products/i-bet151-gsk1210151a.html selleck inhibitor] Valsartan treatment did not affect this response, whereas fasudil treatment markedly enhanced the contraction of aortic segments compared to the l-NAME-evoked hypertensive group. Endothelium-dependent relaxation of aortic rings precontracted with NE was shown in Fig. 4A. Exposure to cumulative concentrations of acetylcholine (Ach) led to a marked vasorelaxation of NE-constricted rings in the control group. In contrast, the response of aortic rings from the model group to Ach was almost abolished, indicating an impaired endothelium-dependent relaxation of the aorta in the NO-deficient rats induced by l-NAME treatment. Little improvement of this effect was observed in the valsartan-treated group, but a significantly improved vasorelaxation was provided by fasudil therapy in comparison to the model group (P