ArticleAmerican journal of physiology. Renal physiology2012
Angiotensin II stimulates epithelial sodium channels in the cortical collecting duct of the rat kidney.
Article in American journal of physiology. Renal physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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63 citing papers in PubMed, 96 citations in OpenAlex.
- Article
- Hypomagnesaemia-associated hypokalaemia requires activation of both ENaC and ROMK.The Journal of physiology · 2025Article
- Review
- NADPH oxidases: redox regulation of cell homeostasis and disease.Physiological reviews · 2025Review
- Luminal flow in the connecting tubule induces afferent arteriole vasodilation.Clinical and experimental nephrology · 2025Article
- Angiotensin II-Type-1a Receptor and Renal K + Wasting during Overnight Low-Na + Intake.Journal of the American Society of Nephrology : JASN · 2024Article
- Luminal Flow in the Connecting Tubule induces Afferent Arteriole Vasodilation.bioRxiv : the preprint server for biology · 2024Article
- A Possible Link between Cell Plasticity and Renin Expression in the Collecting Duct: A Narrative Review.International journal of molecular sciences · 2024Review
- Epithelial NaComprehensive Physiology · 2024Review
- Angiotensin II acts through Rac1 to upregulate pendrin: role of NADPH oxidase.American journal of physiology. Renal physiology · 2024Article
- Mice lacking γENaC palmitoylation sites maintain benzamil-sensitive Na+ transport despite reduced channel activity.JCI insight · 2023Article
- Mutagenesis of the cleavage site of (pro)renin receptor abrogates aldosterone-salt-induced hypertension and renal injury in mice.American journal of physiology. Renal physiology · 2023Article
- Obesity-associated cardiometabolic complications in polycystic ovary syndrome: The potential role of sodium-glucose cotransporter-2 inhibitors.Frontiers in endocrinology · 2023Review
- NOXA1-dependent NADPH oxidase 1 signaling mediates angiotensin II activation of the epithelial sodium channel.American journal of physiology. Renal physiology · 2022Article
- Blood pressure effects of sodium transport along the distal nephron.Kidney international · 2022Review
- Renal NOXA1/NOX1 Signaling Regulates Epithelial Sodium Channel and Sodium Retention in Angiotensin II-induced Hypertension.Antioxidants & redox signaling · 2022Article
- The evolving complexity of the collecting duct renin-angiotensin system in hypertension.Nature reviews. Nephrology · 2021Review
- Renal Dopamine Receptors and Oxidative Stress: Role in Hypertension.Antioxidants & redox signaling · 2021Review
- 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
- Angiotensin II-induced superoxide and decreased glutathione in proximal tubules: effect of dietary fructose.American journal of physiology. Renal physiology · 2020Article
3 more citing papers are in PubMed but not listed here.
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3 authors at 1 institution in 1 country.
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Abstract
We examined the effect of angiotensin II (ANG II) on epithelial Na(+) channel (ENaC) in the rat cortical collecting duct (CCD) with single-channel and the perforated whole cell patch-clamp recording. Application of 50 nM ANG II increased ENaC activity, defined by NP(o) (a product of channel numbers and open probability), and the amiloride-sensitive whole cell Na currents by twofold. The stimulatory effect of ANG II on ENaC was absent in the presence of losartan, suggesting that the effect of ANG II on ENaC was mediated by ANG II type 1 receptor. Moreover, depletion of intracellular Ca(2+) with 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA)-AM failed to abolish the stimulatory effect of ANG II on ENaC but inhibiting protein kinase C (PKC) abolished the effect of ANG II, suggesting that the effect of ANG II was the result of stimulating Ca(2+)-independent PKC. This notion was also suggested by the experiments in which stimulation of PKC with phorbol ester derivative mimicked the effect of ANG II and increased amiloride-sensitive Na currents in the principal cell, an effect that was not abolished by treatment of the CCD with BAPTA-AM. Also, inhibition of NADPH oxidase (NOX) with diphenyleneiodonium chloride abolished the stimulatory effect of ANG II on ENaC and application of superoxide donors, pyrogallol or xanthine and xanthine oxidase, significantly increased ENaC activity. Moreover, addition of ANG II or H(2)O(2) diminished the arachidonic acid (AA)-induced inhibition of ENaC in the CCD. We conclude that ANG II stimulates ENaC in the CCD through a Ca(2+)-independent PKC pathway that activates NOX thereby increasing superoxide generation. The stimulatory effect of ANG II on ENaC may be partially the result of blocking AA-induced inhibition of ENaC.
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