ArticleClinical and experimental nephrology2013
The intercalated cells of the mouse kidney OMCD(is) are the target of the vasopressin V1a receptor axis for urinary acidification.
Article in Clinical and experimental nephrology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- Not all kidney cysts are created equal: a distinct renal cystogenic mechanism in tuberous sclerosis complex (TSC).Frontiers in physiology · 2023Review
- Arginine Vasopressin Modulates Ion and Acid/Base Balance by Regulating Cell Numbers of Sodium Chloride Cotransporter and HInternational journal of molecular sciences · 2020Article
- Osmotic diuresis by SGLT2 inhibition stimulates vasopressin-induced water reabsorption to maintain body fluid volume.Physiological reports · 2020Article
- Vasopressin Increases Urinary AcidificationJournal of the American Society of Nephrology : JASN · 2019Article
- Unraveling the Physiology of (Pro)Renin Receptor in the Distal Nephron.Hypertension (Dallas, Tex. : 1979) · 2017Review
- TSS-Seq analysis of low pH-induced gene expression in intercalated cells in the renal collecting duct.PloS one · 2017Article
- Stimulation of V1a receptor increases renal uric acid clearance via urate transporters: insight into pathogenesis of hypouricemia in SIADH.Clinical and experimental nephrology · 2016Article
- pH-sensitive expression of calcium-sensing receptor (CaSR) in type-B intercalated cells of the cortical collecting ducts (CCD) in mouse kidney.Clinical and experimental nephrology · 2015Article
- Effects of atrial natriuretic peptide on bicarbonate transport in long- and short-looped medullary thick ascending limbs of rats.PloS one · 2013Article
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Authors and funding
9 authors at 4 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundVasopressin V1a receptor (V1aR) null mice have insufficient acid-base balance, but the target cell for V1aR signaling which results in the urinary acidification has not been identified.
methodsBy using a quantitative in situ hybridization technique and a double-staining technique with an anti-AQP3 antibody in mice, we investigated the axial distribution and acidosis-induced expression of V1aR mRNA along the nephron. We also investigated the acidosis-induced morphological change in the tubule cells from wild-type and V1aR-null (V1aR(-/-)) mice.
resultsIn the normal condition, V1aR mRNA was moderately expressed in the medullary thick ascending limb (MTAL) and highly expressed in the intercalated cell (IC) throughout the collecting duct (CD). However, no expression was observed in the proximal tubule, thin limbs of Henle's loop, and the principal cell of the CD. Importantly, V1aR mRNA was upregulated significantly both in the TAL and the IC of the CD in the inner stripe of the outer medulla (MTALis and IC of OMCDis, respectively) when mice were treated with NH4Cl (0.28 mol/L) for 6 days. Acidosis-induced hypertrophy, which was completely attenuated in V1aR(-/-) mice, was observed only in the IC of OMCDis (P < 0.005). In addition, urinary excretion of ammonia (NH3/NH4 (+)) was significantly decreased on day 3 (P < 0.05) and day 6 (P < 0.005) in the V1aR(-/-) mice treated with NH4Cl.
conclusionIn conclusion, the IC of OMCDis may be the target cell stimulated by the vasopressin V1aR axis and contribute to urinary acidification, at least during metabolic acidosis.
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