ArticleThe Journal of biological chemistry2011
Diminished paracrine regulation of the epithelial Na+ channel by purinergic signaling in mice lacking connexin 30.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 43 citations in OpenAlex.
- GPER1 activation regulates renal purinergic P2YAmerican journal of physiology. Regulatory, integrative and comparative physiology · 2026Article
- P2YInternational journal of molecular sciences · 2025Review
- Epithelial NaComprehensive Physiology · 2024Review
- P2Y2 receptor decreases blood pressure by inhibiting ENaC.JCI insight · 2023Article
- Aldosterone: Renal Action and Physiological Effects.Comprehensive Physiology · 2023Article
- Extracellular Nucleotides and P2 Receptors in Renal Function.Physiological reviews · 2020Review
- Intercalated Cells of the Kidney Collecting Duct in Kidney Physiology.Seminars in nephrology · 2019Review
- Renal NaAmerican journal of physiology. Renal physiology · 2019Article
- ATP Release Channels.International journal of molecular sciences · 2018Review
- Acute In Vivo Analysis of ATP Release in Rat Kidneys in Response to Changes of Renal Perfusion Pressure.Journal of the American Heart Association · 2017Article
- ENaC activity in the cortical collecting duct of HKαAmerican journal of physiology. Renal physiology · 2017Article
- Functional roles of connexins and pannexins in the kidney.Cellular and molecular life sciences : CMLS · 2015Review
- Relative roles of principal and intercalated cells in the regulation of sodium balance and blood pressure.Current hypertension reports · 2015Review
- Purinergic signalling in the kidney in health and disease.Purinergic signalling · 2014Review
- Opening lines of communication in the distal nephron.The Journal of clinical investigation · 2013Article
- Renal β-intercalated cells maintain body fluid and electrolyte balance.The Journal of clinical investigation · 2013Article
- ATP releasing connexin 30 hemichannels mediate flow-induced calcium signaling in the collecting duct.Frontiers in physiology · 2013Article
- Recording ion channels in isolated, split-opened tubules.Methods in molecular biology (Clifton, N.J.) · 2013Article
- Intrarenal localization of the plasma membrane ATP channel pannexin1.American journal of physiology. Renal physiology · 2012Article
- Flow-sensitive K+-coupled ATP secretion modulates activity of the epithelial Na+ channel in the distal nephron.The Journal of biological chemistry · 2012Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
We tested whether ATP release through Connexin 30 (Cx30) is part of a local purinergic regulatory system intrinsic to the aldosterone-sensitive distal nephron (ASDN) important for proper control of sodium excretion; if changes in sodium intake influence ATP release via Cx30; and if this allows a normal ENaC response to changes in systemic sodium levels. In addition, we define the consequences of disrupting ATP regulation of ENaC in Cx30(-/-) mice. Urinary ATP levels in wild-type mice increase with sodium intake, being lower and less dependent on sodium intake in Cx30(-/-) mice. Loss of inhibitory ATP regulation causes ENaC activity to be greater in Cx30(-/-) versus wild-type mice, particularly with high sodium intake. This results from compromised ATP release rather than end-organ resistance: ENaC in Cx30(-/-) mice responds to exogenous ATP. Thus, loss of paracrine ATP feedback regulation of ENaC in Cx30(-/-) mice disrupts normal responses to changes in sodium intake. Consequently, ENaC is hyperactive in Cx30(-/-) mice lowering sodium excretion particularly during increases in sodium intake. Clamping mineralocorticoids high in Cx30(-/-) mice fed a high sodium diet causes a marked decline in renal sodium excretion. This is not the case in wild-type mice, which are capable of undergoing aldosterone-escape. This loss of the ability of ENaC to respond to changes in sodium levels contributes to salt-sensitive hypertension in Cx30(-/-) mice.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.