ArticleAmerican journal of physiology. Renal physiology2015
Prolactin stimulates sodium and chloride ion channels in A6 renal epithelial cells.
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 6 papers.
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Who cites it
6 citing papers in PubMed, 15 citations in OpenAlex.
- Interactions Between Prolactin, Intracellular Signaling, and Possible Implications in the Contractility and Pathophysiology of Asthma.International journal of molecular sciences · 2025Review
- Sheehan syndrome: a current approach to a dormant disease.Pituitary · 2025Review
- Multiple cell types in the oviduct express the prolactin receptor.FASEB bioAdvances · 2022Article
- Secretion and Function of Pituitary Prolactin in Evolutionary Perspective.Frontiers in neuroscience · 2020Review
- Volume regulatory hormones and plasma volume in pregnant women with sickle cell disorder.Journal of the renin-angiotensin-aldosterone system : JRAAS · 2016Article
- Electrolyte Imbalance in Patients with Sheehan's Syndrome.Endocrinology and metabolism (Seoul, Korea) · 2015Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Many hormonal pathways contribute to the regulation of renal epithelial sodium channel (ENaC) function, a key process for maintaining blood volume and controlling blood pressure. In the present study, we examined whether the peptide hormone prolactin (PRL) regulates ENaC function in renal epithelial cells (A6). Basolateral application of several different concentrations of PRL dramatically stimulated the transepithelial current in A6 cells, increasing both amiloride-sensitive (ENaC) and amiloride-insensitive currents. Using cell-attached patch clamp, we determined that PRL increased both the number (N) and open probability (Po) of ENaC present in the apical membrane. Inhibition of PKA with H-89 abolished the effect of PRL on amiloride-sensitive and insensitive transepithelial currents and eliminated the increase in ENaC NPo with PRL exposure. PRL also increased cAMP in A6 cells, consistent with signaling through the cAMP-dependent PKA pathway. We also identified that PRL induced activity of a 2-pS anion channel with outward rectification, electrophysiological properties consistent with ClC4 or ClC5. RT-PCR only detected ClC4, but not ClC5 transcripts. Here, we show for the first time that PRL activates sodium and chloride transport in renal epithelial cells via ENaC and ClC4.
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Registered trials
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