ArticleHypertension (Dallas, Tex. : 1979)2013
Chronic angiotensin II infusion drives extensive aldosterone-independent epithelial Na+ channel activation.
Article in Hypertension (Dallas, Tex. : 1979), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 62 citations in OpenAlex.
- Article
- Intercalated Cell ClC-K2 Channel Contributes to Systemic ClFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Aldosterone Antagonism Is More Effective at Reducing Blood Pressure and Excessive Renal ENaC Activity in AngII-Infused Female Rats Than in Males.Hypertension (Dallas, Tex. : 1979) · 2023Article
- NOXA1-dependent NADPH oxidase 1 signaling mediates angiotensin II activation of the epithelial sodium channel.American journal of physiology. Renal physiology · 2022Article
- Bile acids regulate the epithelial NaThe Journal of physiology · 2022Article
- Cell-Specific Actions of the Prostaglandin E-Prostanoid Receptor 4 Attenuating Hypertension: A Dominant Role for Kidney Epithelial Cells Compared With Macrophages.Journal of the American Heart Association · 2022Article
- Kidney-Specific CAP1/Prss8-Deficient Mice Maintain ENaC-Mediated Sodium Balance through an Aldosterone Independent Pathway.International journal of molecular sciences · 2022Article
- Renal NOXA1/NOX1 Signaling Regulates Epithelial Sodium Channel and Sodium Retention in Angiotensin II-induced Hypertension.Antioxidants & redox signaling · 2022Article
- Epac1-/- and Epac2-/- mice exhibit deficient epithelial Na+ channel regulation and impaired urinary Na+ conservation.JCI insight · 2022Article
- The evolving complexity of the collecting duct renin-angiotensin system in hypertension.Nature reviews. Nephrology · 2021Review
- α-Ketoglutarate Upregulates Collecting Duct (Pro)renin Receptor Expression, Tubular Angiotensin II Formation, and NaFrontiers in cardiovascular medicine · 2021Article
- Osmotic Adaptation by NaBiomedicines · 2020Review
- Electrolyte and transporter responses to angiotensin II induced hypertension in female and male rats and mice.Acta physiologica (Oxford, England) · 2020Article
- Effect of Angiotensin II on ENaC in the Distal Convoluted Tubule and in the Cortical Collecting Duct of Mineralocorticoid Receptor Deficient Mice.Journal of the American Heart Association · 2020Article
- Effects of ATRAP in Renal Proximal Tubules on Angiotensin-Dependent Hypertension.Journal of the American Heart Association · 2019Article
- Potassium Intake Prevents the Induction of the Renin-Angiotensin System and Increases Medullary ACE2 and COX-2 in the Kidneys of Angiotensin II-Dependent Hypertensive Rats.Frontiers in pharmacology · 2019Article
- Deficient transient receptor potential vanilloid type 4 function contributes to compromised [CaFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Angiotensin II Signal Transduction: An Update on Mechanisms of Physiology and Pathophysiology.Physiological reviews · 2018Review
- Dietary KPflugers Archiv : European journal of physiology · 2018Article
- Collecting duct prorenin receptor knockout reduces renal function, increases sodium excretion, and mitigates renal responses in ANG II-induced hypertensive mice.American journal of physiology. Renal physiology · 2017Article
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7 authors at 1 institution in 1 country.
Funding
Abstract
The inability of mineralocorticoid receptor (MR) blockade to reduce hypertension associated with high angiotensin (Ang) II suggests direct actions of Ang II to regulate tubular sodium reabsorption via the epithelial Na(+) channel (ENaC) in the aldosterone-sensitive distal nephron. We used freshly isolated aldosterone-sensitive distal nephron from mice to delineate the synergism and primacy between aldosterone and Ang II in controlling functional ENaC activity. Inhibition of MR specifically prevented the increased number of functionally active ENaC, but not ENaC open probability elicited by a low sodium diet. In contrast, we found no functional role of glucocorticoid receptors in the regulation of ENaC activity by dietary salt intake. Simultaneous inhibition of MR and Ang II type 1 receptors ameliorated the enhanced ENaC activity caused by low dietary salt intake and produced significantly greater natriuresis than either inhibitor alone. Chronic systemic Ang II infusion induced more than 2 times greater increase in ENaC activity than observed during dietary sodium restriction. Importantly, ENaC activity remained greatly above control levels during maximal MR inhibition. We conclude that during variations in dietary salt intake both aldosterone and Ang II contribute complementarily to the regulation of ENaC activity in the aldosterone-sensitive distal nephron. In contrast, in the setting of Ang II-dependent hypertension, ENaC activity is upregulated well above the physiological range and is not effectively suppressed by inhibition of the aldosterone-MR axis. This provides a mechanistic explanation for the resistance to MR inhibition that occurs in hypertensive subjects having elevated intrarenal Ang II levels.
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