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Tytuł:
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NaHCO 3 Dilates Mouse Afferent Arteriole Via Na Cotransporters NBCs.
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Autorzy:
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Jiang S; From Kidney Disease Center, the First Affiliated Hospital, and Department of Physiology, School of Basic Medical Sciences, Zhejiang University School of Medicine, Hangzhou, China (S.J., G.Z., P.X., L.Z., L.L., J.C., E.Y.L.).; Department of Molecular Pharmacology and Physiology, University of South Florida College of Medicine, Tampa (S.J., X.W., J.W., G.Z., J.Z., L.W., R.L.).
Wang X; Department of Molecular Pharmacology and Physiology, University of South Florida College of Medicine, Tampa (S.J., X.W., J.W., G.Z., J.Z., L.W., R.L.).; Shandong Provincial Hospital, Affiliated Hospital of Shandong University, Jinan, China (X.W.).
Wei J; Department of Molecular Pharmacology and Physiology, University of South Florida College of Medicine, Tampa (S.J., X.W., J.W., G.Z., J.Z., L.W., R.L.).
Zhang G; From Kidney Disease Center, the First Affiliated Hospital, and Department of Physiology, School of Basic Medical Sciences, Zhejiang University School of Medicine, Hangzhou, China (S.J., G.Z., P.X., L.Z., L.L., J.C., E.Y.L.).; Department of Molecular Pharmacology and Physiology, University of South Florida College of Medicine, Tampa (S.J., X.W., J.W., G.Z., J.Z., L.W., R.L.).
Zhang J; Department of Molecular Pharmacology and Physiology, University of South Florida College of Medicine, Tampa (S.J., X.W., J.W., G.Z., J.Z., L.W., R.L.).
Xie P; From Kidney Disease Center, the First Affiliated Hospital, and Department of Physiology, School of Basic Medical Sciences, Zhejiang University School of Medicine, Hangzhou, China (S.J., G.Z., P.X., L.Z., L.L., J.C., E.Y.L.).
Xu L; College of Public Health, University of South Florida, Tampa (L.X.).
Wang L; Department of Molecular Pharmacology and Physiology, University of South Florida College of Medicine, Tampa (S.J., X.W., J.W., G.Z., J.Z., L.W., R.L.).
Zhao L; From Kidney Disease Center, the First Affiliated Hospital, and Department of Physiology, School of Basic Medical Sciences, Zhejiang University School of Medicine, Hangzhou, China (S.J., G.Z., P.X., L.Z., L.L., J.C., E.Y.L.).; Department of Physiology, School of Basic Medical Sciences, Guangzhou Medical University, China (L.Z., E.Y.L.).; Institute of Vegetative Physiology, Charité-Universitätsmedizin Berlin, Humboldt-Universität zu Berlin, Germany (L.Z., E.Y.L.).
Li L; From Kidney Disease Center, the First Affiliated Hospital, and Department of Physiology, School of Basic Medical Sciences, Zhejiang University School of Medicine, Hangzhou, China (S.J., G.Z., P.X., L.Z., L.L., J.C., E.Y.L.).; Division of Nephrology and Hypertension, and Hypertension Center, Georgetown University, Washington, DC (L.L., C.S.W.).
Wilcox CS; Division of Nephrology and Hypertension, and Hypertension Center, Georgetown University, Washington, DC (L.L., C.S.W.).
Chen J; From Kidney Disease Center, the First Affiliated Hospital, and Department of Physiology, School of Basic Medical Sciences, Zhejiang University School of Medicine, Hangzhou, China (S.J., G.Z., P.X., L.Z., L.L., J.C., E.Y.L.).
Lai EY; From Kidney Disease Center, the First Affiliated Hospital, and Department of Physiology, School of Basic Medical Sciences, Zhejiang University School of Medicine, Hangzhou, China (S.J., G.Z., P.X., L.Z., L.L., J.C., E.Y.L.).; Department of Physiology, School of Basic Medical Sciences, Guangzhou Medical University, China (L.Z., E.Y.L.).; Institute of Vegetative Physiology, Charité-Universitätsmedizin Berlin, Humboldt-Universität zu Berlin, Germany (L.Z., E.Y.L.).
Liu R; Department of Molecular Pharmacology and Physiology, University of South Florida College of Medicine, Tampa (S.J., X.W., J.W., G.Z., J.Z., L.W., R.L.).
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Źródło:
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Hypertension (Dallas, Tex. : 1979) [Hypertension] 2019 Nov; Vol. 74 (5), pp. 1104-1112. Date of Electronic Publication: 2019 Sep 16.
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Typ publikacji:
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Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
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Język:
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English
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Imprint Name(s):
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Publication: : Hagerstown, MD : Lippincott, Williams & Wilkins
Original Publication: [Dallas, Tex.] : [American Heart Association], [©1979]-
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MeSH Terms:
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Arterioles/*drug effects
Kidney Glomerulus/*drug effects
Sodium Bicarbonate/*pharmacology
Sodium-Bicarbonate Symporters/*metabolism
Vasodilation/*drug effects
Animals ; Arterioles/physiology ; Disease Models, Animal ; Glomerular Filtration Rate/drug effects ; Male ; Mice ; Mice, Inbred C57BL ; Nitric Oxide/metabolism ; Perfusion/methods ; Renal Insufficiency, Chronic/drug therapy ; Renal Insufficiency, Chronic/pathology ; Sensitivity and Specificity ; Sodium-Bicarbonate Symporters/drug effects ; Tissue Culture Techniques ; Vasodilation/physiology
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Grant Information:
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R01 DK099276 United States DK NIDDK NIH HHS; R01 HL137987 United States HL NHLBI NIH HHS; R01 HL142814 United States HL NHLBI NIH HHS
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Contributed Indexing:
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Keywords: arterioles; glomerular filtration rate; nitric oxide; sodium bicarbonate; vasodilation
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Substance Nomenclature:
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0 (Sodium-Bicarbonate Symporters)
31C4KY9ESH (Nitric Oxide)
8MDF5V39QO (Sodium Bicarbonate)
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Entry Date(s):
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Date Created: 20190917 Date Completed: 20191120 Latest Revision: 20201101
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Update Code:
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20240105
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PubMed Central ID:
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PMC6785401
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DOI:
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10.1161/HYPERTENSIONAHA.119.13235
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PMID:
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31522618
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Sodium bicarbonate has long been used to treat chronic kidney disease. It has been demonstrated to slow the decline in glomerular filtration rate in chronic kidney disease patient; however, the mechanisms are not completely understood. We hypothesized that NaHCO 3 dilates afferent arterioles (Af-Art) by stimulating nitric oxide (NO) release mediated by the Na + /HCO 3 - cotransporter (NBC) contributing to the elevation in glomerular filtration rate. Isolated microperfused mouse renal Af-Art, preconstricted with norepinephrine (1 µmol/L), dilated 45±2% (n=6, P <0.05) in response to NaHCO 3 (44 mmol/L). Whereas, NaCl solution containing the same Na + concentration was not effective. The mRNA for NBCn1 and NBCe1 were detected in microdissected Af-Art using reverse transcription-polymerase chain reaction and quantitative polymerase chain reaction. The Af-Art intracellular pH measured with 2',7'-bis-(2-carboxyethyl)-5-(and-6) carboxyfluorescein, acetoxymethyl ester increased significantly by 0.29±0.02 (n=6; P <0.05) in the presence of NaHCO 3 , which was blunted by N-cyanosulphonamide compound (S0859) that is an inhibitor of the NBC family. After clamping the intracellular pH with 10 μM nigericin, changing the bath solution pH from 7.4 to 7.8 still dilates the Af-Art by 53±4% (n=7; P <0.005) and increases NO generation by 22±3% (n=7; P <0.005). Both pH-induced NO generation and vasodilation were blocked by L-NG-Nitroarginine Methyl Ester. NaHCO 3 increased NO generation in Af-Art by 19±4% (n=5; P <0.005) and elevated glomerular filtration rate in conscious mice by 36% (233 versus 318 ul/min; n=9-10; P <0.0001). S0859 and L-NG-nitroarginine methyl ester blocked NaHCO 3 -induced increases in NO generation and vasodilation. We conclude that NBCn1 and NBCe1 are expressed in Af-Art and that NaHCO 3 dilates Af-Art via NBCs mediated by NO that increases the glomerular filtration rate.
