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INTRODUCTION: ). METHODS: rats were examined to determine changes in blood pressure and kidney function with increased sodium chloride intake. Kidney microvasculature was examined for changes in expression of key regulatory contractile proteins and autoregulatory function in vivo and effects of CCL2 on function in vitro. RESULTS: rats. Kidney microvascular smooth muscle cells undergoing cyclic strain produced CCL2 that decreased expression of Notch3 and myosin light chain kinase (Mylk). Addition of recombinant CCL2 to medium of kidney microvascular smooth muscle cells promoted dose-dependent decreases in mRNA expression of Notch3 and Mylk, and MLCK and p-MLC2 proteins. CONCLUSIONS: CCL2 directly impairs kidney microvascular smooth muscle contractility, leading to autoregulatory dysfunction and kidney injury in hypertensive SS rats. The findings highlight CCL2 as a potential therapeutic target in hypertensive nephropathy.
Feng et al. (Sat,) studied this question.