Abstract
This study explores the role of inducible nitric oxide synthase (iNOS) in the pathogenesis of diabetes mellitus-induced erectile dysfunction (DMED) and the effect of angiotensin 1–7 (Ang- [1–7]) on NOS levels. A type 2 diabetes mellitus (DM) rat model was established. Erectile function was assessed by measuring intracavernous pressure and mean arterial pressure after electrical stimulation. The expression of iNOS, endothelial NOS (eNOS), eNOS phosphorylated at Ser 1177 (p-eNOS [Ser 1177]), and AKT/p-AKT in corpus cavernosum smooth muscle cells (CCSMCs) was measured by Western blotting and immunofluorescence. The plasma levels of NO, SOD, malondialdehyde, and peroxynitrite were calculated. Intracellular calcium content was determined by flow cytometry. DMED rats exhibited decreased erectile function and severe oxidative stress. Ang-(1−7) treatment improved erectile response and suppressed oxidative stress by upregulating p-eNOS/eNOS and downregulating iNOS levels. Silencing iNOS in CCSMCs decreased oxidative stress and intracellular calcium levels induced by high glucose. In turn, iNOS overexpression increased oxidative stress and intracellular calcium level. Treatment with the MAS receptor antagonist A779 and the Akt antagonist LY294002 reversed the effects of Ang-(1−7) on iNOS. Ang-(1−7) improved DMED through the MAS/AKT signaling pathway.
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