Monosodium glutamate altered renal architecture and modulated expression of NMDA-R, eNOS, and nNOS in normotensive and hypertensive rats.

Monosodium glutamate (MSG) administration has been shown to pronounce hypertension and oxidative status with increased renal blood flow (RBF), however, the precise mechanisms of action have never been demonstrated. This study aimed to investigate the MSG action by studying the alteration in renal architecture and specific protein expression in 2-kidney-1-clip hypertensive comparing to sham operative normotensive rats. The administered doses of MSG were 80, 160, or 320 mg/kg BW daily for 8 weeks. Using routine chemical staining, the congestion of glomerular capillaries, a lesser renal corpuscles and glomeruli size, a widen Bowman capsule's space, an increase in mesangial cell proliferation and mesangial matrix, renal interstitial fibrosis, focal cloudy swelling of renal tubular epithelial cells were observed. Immunological study revealed an increase in the expression of N-methyl-D-aspartate receptor (NMDA-R) and endothelial nitric oxide synthase (eNOS) but a decrease in neuronal NOS (nNOS). It is suggested that MSG may upregulate the NMDA-R levels which responsible for the oxidative stress, glomerular injury, and renal interstitial fibrosis. The NMDA-R may also stimulate eNOS overexpression which resulted in renal microvascular dilatation, a raise in RBF and GFR, and natriuresis and diuresis promotion. Long-term exposure of MSG may trigger adaptation of tubuloglomerular feedback through nNOS downregulation.