Renal NCC is unchanged in the midpregnant rat and decreased in the late pregnant rat despite avid renal Na+ retention

摘要: Pregnancy is characterized by plasma volume expansion due to Na+ retention, driven aldosterone. The aldosterone-responsive epithelial channel activated in the kidney pregnancy. In present study, we investigated Na+-Cl− cotransporter (NCC) mid- and late pregnant rats compared with virgin rats. We determined abundance of total NCC, phosphorylated NCC (pNCC; pT53, pS71 pS89), STE20/SPS-1-related proline-alanine-rich protein kinase (pSPAK; pS373), oxidative stress-related (pOSR1; pS325) cortex. also measured mRNA expression members SPAK/NCC regulatory network, serum glucocorticoid-regulated (SGK)1, no lysine (WNK)1, WNK3, WNK4. Additionally, performed immunohistochemistry for kidneys from Total pNCC, pSPAK/OSR1 were unchanged midpregnant versus rats, pNCC decreased; however, was unchanged. detected differences SGK1, WNK1, By immunohistochemistry, mainly localized apical region density reduced Therefore, despite high circulating aldosterone levels pregnancy, transporter not increased or (phosphorylated) localization all are This contrasts mineralocorticoid-mediated activation channel, which have previously reported. Why how escapes pregnancy clear but may relate regional sensitivity K+ intake other undefined mechanisms.