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Downregulation of vasopressin V1A receptors and activation of mitogen‐activated protein kinase in rat mesangial cells cultured under high‐glucose conditions

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Summary

In the present study we examined the effects of high extracellular glucose concentrations on vasopressin (AVP) V1A receptor kinetics and signal transduction in cultured rat mesangial cells. Scatchard analysis of [3H]‐AVP binding to mesangial cell plasma membranes showed that although high glucose (30 mmol/L) decreased V1A receptor numbers relative to cells cultured in normal glucose (10 mmol/L), receptor affinity was not affected. This V1A receptor downregulation was associated with an attenuated increase in AVP‐stimulated cytosolic free calcium concentrations ([Ca2+]i). In addition, high glucose increased both the basal and AVP‐stimulated activity of the classic mitogen‐activated protein kinase, namely extracellular signal‐regulated kinase (ERK). Furthermore, high glucose induced activation of protein kinase C (PKC) in mesangial cells that could be inhibited by coincubation with the PKC inhibitor staurosporine (10 nmol/L). Staurosporine also markedly attenuated the high glucose‐induced downregulation of V1A receptors on mesangial cells and blocked the depressed [Ca2+]i response and increased ERK activity induced by AVP. The results indicate that high extracellular glucose downregulates V1A receptors on rat mesangial cells and modulates their signal transduction properties via PKC activation.
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Document Type: Research Article

Publication date: May 1, 2012

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