Abstract

Reactive oxygen species (ROS) can increase contractile responses in hypertensive rat vessels. This study aimed to evaluate the role of the endothelial cells (EC) and ROS to the contraction induced by phenylephrine (PE) in aorta from renal hypertensive (2K‐1C) and normotensive rat (2K). Concentration‐effect curves for PE were constructed in intact endothelium (E+) and denuded aorta (E−), with or without Catalase. Expression of phosphorylated Ser1177eNOS was evaluated by Western‐Blot. In isolated EC incubated with PE, it was measured the fluorescence intensity (FI) of the ROS sensitive dye (DHE) by flow citometry, with or without Catalase. The H2O2 production was measured through assay kit. The maximum contraction to PE was decreased only in 2K‐1C E+, which was partially reversed by Catalase. PE induces higher Ser1177phosphorylation of eNOS in 2K‐1C aorta than in 2K. PE increased the FI only in EC from 2K‐1C, and it was abolished by Catalase. PE stimulated higher H2O2 production in 2K‐1C (E+) than in 2K (E+). In conclusion, the reduced contraction to PE in E+ rat aorta from 2K‐1C is due to high eNOS‐Ser1177 phosphorylation and H2O2 production in the EC. Supported by FAPESP, CAPES and CNPq.

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