ArticleAmerican journal of physiology. Renal physiology2015
Renal NCC is unchanged in the midpregnant rat and decreased in the late pregnant rat despite avid renal Na+ retention.
Article in American journal of physiology. Renal physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- Sex differences in renal transporters: assessment and functional consequences.Nature reviews. Nephrology · 2024Review
- Effect of pregnancy and hypertension on kidney function in female rats: Modeling and functional implications.PloS one · 2023Article
- Renal KFrontiers in physiology · 2023Review
- Time course of renal sodium transport in the pregnant rat.Current research in physiology · 2021Article
- Renal and colonic potassium transporters in the pregnant rat.American journal of physiology. Renal physiology · 2018Article
- Sexual Dimorphic Pattern of Renal Transporters and Electrolyte Homeostasis.Journal of the American Society of Nephrology : JASN · 2017Article
- The enigma of continual plasma volume expansion in pregnancy: critical role of the renin-angiotensin-aldosterone system.American journal of physiology. Renal physiology · 2016Review
- The chloride-bicarbonate exchanger pendrin is increased in the kidney of the pregnant rat.Experimental physiology · 2015Article
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5 authors at 3 institutions in 1 country.
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Abstract
Pregnancy is characterized by plasma volume expansion due to Na(+) retention, driven by aldosterone. The aldosterone-responsive epithelial Na(+) channel is activated in the kidney in pregnancy. In the present study, we investigated the aldosterone-responsive Na(+)-Cl(-) cotransporter (NCC) in mid- and late pregnant rats compared with virgin rats. We determined the abundance of total NCC, phosphorylated NCC (pNCC; pT53, pS71 and pS89), phosphorylated STE20/SPS-1-related proline-alanine-rich protein kinase (pSPAK; pS373), and phosphorylated oxidative stress-related kinase (pOSR1; pS325) in the kidney cortex. We also measured mRNA expression of NCC and members of the SPAK/NCC regulatory kinase network, serum and glucocorticoid-regulated kinase (SGK)1, total with no lysine kinase (WNK)1, WNK3, and WNK4. Additionally, we performed immunohistochemistry for NCC kidneys from virgin and pregnant rats. Total NCC, pNCC, and pSPAK/OSR1 abundance were unchanged in midpregnant versus virgin rats. In late pregnant versus virgin rats, total NCC and pNCC were decreased; however, pSPAK/OSR1 was unchanged. We detected no differences in mRNA expression of NCC, SGK1, total WNK1, WNK3, and WNK4. By immunohistochemistry, NCC was mainly localized to the apical region in virgin rats, and density in the apical region was reduced in late pregnancy. Therefore, despite high circulating aldosterone levels in pregnancy, the aldosterone-responsive transporter NCC is not increased in total or activated (phosphorylated) abundance or in apical localization in midpregnant rats, and all are reduced in late pregnancy. This contrasts to the mineralocorticoid-mediated activation of the epithelial Na(+) channel, which we have previously reported. Why and how NCC escapes aldosterone activation in pregnancy is not clear but may relate to regional differences in aldosterone sensitivity the increased K(+) intake or other undefined mechanisms.
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