ArticleAmerican journal of physiology. Cell physiology2011
Aldosterone stimulates vacuolar H(+)-ATPase activity in renal acid-secretory intercalated cells mainly via a protein kinase C-dependent pathway.
Article in American journal of physiology. Cell physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 50 citations in OpenAlex.
- Aldosterone: From Essential Tubular Regulator to Pathological Driver-Physiology, Disease, and Therapeutic Advances.International journal of molecular sciences · 2025Review
- Combined effect of esaxerenone and dapagliflozin on aldosterone-mediated sodium reabsorption and potassium excretion.Frontiers in physiology · 2025Article
- The Role of the Endocrine System in the Regulation of Acid-Base Balance by the Kidney and the Progression of Chronic Kidney Disease.International journal of molecular sciences · 2024Review
- Aldosterone: Renal Action and Physiological Effects.Comprehensive Physiology · 2023Article
- Regulation of Rhcg, an ammonia transporter, by aldosterone in the kidney.The Journal of endocrinology · 2021Article
- Article
- Adhesion-GPCR Gpr116 (ADGRF5) expression inhibits renal acid secretion.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Vasopressin Increases Urinary AcidificationJournal of the American Society of Nephrology : JASN · 2019Article
- Pathophysiology, diagnosis and treatment of inherited distal renal tubular acidosis.Journal of nephrology · 2018Review
- The ammonia transporter RhCG modulates urinary acidification by interacting with the vacuolar proton-ATPases in renal intercalated cells.Kidney international · 2018Article
- Characterization and Correction of Olfactory Deficits in Kidney Disease.Journal of the American Society of Nephrology : JASN · 2017Article
- Article
- GnRH Neuron-Specific Ablation of Gαq/11 Results in Only Partial Inactivation of the Neuroendocrine-Reproductive Axis in Both Male and Female Mice: In Vivo Evidence for Kiss1r-Coupled Gαq/11-Independent GnRH Secretion.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Aldosterone Disrupts the Intercellular Flow of Glucose in Cardiac Muscle.Frontiers in endocrinology · 2015Article
- Renal type a intercalated cells contain albumin in organelles with aldosterone-regulated abundance.PloS one · 2015Article
- Molecular mechanisms and regulation of urinary acidification.Comprehensive Physiology · 2014Review
- Uroguanylin inhibits H-ATPase activity and surface expression in renal distal tubules by a PKG-dependent pathway.American journal of physiology. Cell physiology · 2014Article
- Everything you need to know about distal renal tubular acidosis in autoimmune disease.Rheumatology international · 2014Review
- The intercalated cells of the mouse kidney OMCD(is) are the target of the vasopressin V1a receptor axis for urinary acidification.Clinical and experimental nephrology · 2013Article
- Connecting type A intercalated cell metabolic state to V-ATPase function: phosphorylation does matter!American journal of physiology. Renal physiology · 2013Article
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Authors and funding
9 authors at 4 institutions in 4 countries.
Funding
Abstract
Urinary acidification in the collecting duct is mediated by the activity of H(+)-ATPases and is stimulated by various factors including angiotensin II and aldosterone. Classically, aldosterone effects are mediated via the mineralocorticoid receptor. Recently, we demonstrated a nongenomic stimulatory effect of aldosterone on H(+)-ATPase activity in acid-secretory intercalated cells of isolated mouse outer medullary collecting ducts (OMCD). Here we investigated the intracellular signaling cascade mediating this stimulatory effect. Aldosterone stimulated H(+)-ATPase activity in isolated mouse and human OMCDs. This effect was blocked by suramin, a general G protein inhibitor, and GP-2A, a specific G(αq) inhibitor, whereas pertussis toxin was without effect. Inhibition of phospholipase C with U-73122, chelation of intracellular Ca(2+) with BAPTA, and blockade of protein kinase C prevented the stimulation of H(+)-ATPases. Stimulation of PKC by DOG mimicked the effect of aldosterone on H(+)-ATPase activity. Similarly, aldosterone and DOG induced a rapid translocation of H(+)-ATPases to the luminal side of OMCD cells in vivo. In addition, PD098059, an inhibitor of ERK1/2 activation, blocked the aldosterone and DOG effects. Inhibition of PKA with H89 or KT2750 prevented and incubation with 8-bromoadenosine-cAMP mildly increased H(+)-ATPase activity. Thus, the nongenomic modulation of H(+)-ATPase activity in OMCD-intercalated cells by aldosterone involves several intracellular pathways and may be mediated by a G(αq) protein-coupled receptor and PKC. PKA and cAMP appear to have a modulatory effect. The rapid nongenomic action of aldosterone may participate in the regulation of H(+)-ATPase activity and contribute to final urinary acidification.
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