We are analyzing https://link.springer.com/article/10.1007/bf00595689.

Title:
Rheogenic sodium-bicarbonate cotransport in the peritubular cell membrane of rat renal proximal tubule | Pflügers Archiv - European Journal of Physiology
Description:
The mechanism of bicarbonate transport across the peritubular cell membrane was investigated in rat kidney proximal tubules in situ by measuring cell pH and cell Na+ activity in response to sudden reduction of peritubular Na+ and/or HCO 3 − . The following observations were made: 1. sudden peritubular reduction of either ion concentration produced the same transient depolarizing potential response; 2. bicarbonate efflux in response to peritubular reduction of bicarbonate was accompanied by sodium efflux; 3. sodium efflux in response to peritubular sodium removal was accompanied by cell acidification indicating bicarbonate efflux; 4. all aforementioned phenomena were inhibited by SITS (10−3 mol/l) except for a small SITS-independent sodium efflux and depolarization which occurred in response to peritubular sodium removal and was not accompanied by cell pH changes; 5. bicarbonate efflux and accompanying potential changes in response to reduction of peritubular bicarbonate virtually vanished in sodium-free solutions. From these observations we conclude that bicarbonate efflux proceeds as rheogenic sodium-bicarbonate cotransport with a stoichiometry of bicarbonate to sodium greater than 1. The question which of the charged species of the bicarbonate buffer system moves cannot yet be decided. Attempts to determine the stoichiometry from the SITS-inhibitable initial cell depolarization and from the SITS-inhibitable initial fluxes suggest a stoichiometry of 3 HCO 3 − : 1 Na+. In addition to sodium-dependent bicarbonate flux, evidence was obtained for a sodium-independent transport system of acids or bases which is able to regulate cell pH even in sodium-free solutions.
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Keywords {🔍}

google, scholar, proximal, bicarbonate, cell, rat, frömter, transport, sodium, peritubular, membrane, kidney, renal, tubule, article, pflügers, burckhardt, yoshitomi, efflux, arch, response, hco, ion, intracellular, physiol, privacy, cookies, content, access, tubular, biol, publish, research, search, rheogenic, sodiumbicarbonate, cotransport, reduction, stoichiometry, nah, vesicles, nature, regulation, eds, cells, membr, springer, analysis, data, information,

Topics {✒️}

rheogenic sodium-bicarbonate cotransport sodium-independent transport system month download article/chapter johann wolfgang goethe-universität sodium-dependent bicarbonate flux bicarbonate-dependent process inhibitable renal proximal tubule rat proximal tubule ion selective microelectrode proximal tubular epithelium intracellular ph regulation rat renal cortex atp-driven proton pump thenecturus proximal tubule sodium-free solutions rat small intestine measuring cell ph regulate cell ph sodium bicarbonate administration sodium/proton antiport kidney physiology privacy choices/manage cookies full article pdf basolateral cell membrane peritubular sodium removal rat kidney studied rat kidney cortex peritubular cell membrane brush-border membranes ion concentration produced bicarbonate efflux proceeds check access instant access european economic area exocrine glands published scope submit manuscript intensive care unit electrochemical potential difference national cardiovascular center theodor-stern-kai 7 bicarbonate permeation cell ph conditions privacy policy cell na+ activity hydrogen transport research institute intracellular chloride activity accepting optional cookies sodium efflux steiner ra

Questions {❓}

Yoshitomi K, Frömter E (1985) How big is the electrochemical potential difference of Na+ across rat renal proximal tubular cell membranes in vivo?

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         description:The mechanism of bicarbonate transport across the peritubular cell membrane was investigated in rat kidney proximal tubules in situ by measuring cell pH and cell Na+ activity in response to sudden reduction of peritubular Na+ and/or HCO 3 − . The following observations were made: 1. sudden peritubular reduction of either ion concentration produced the same transient depolarizing potential response; 2. bicarbonate efflux in response to peritubular reduction of bicarbonate was accompanied by sodium efflux; 3. sodium efflux in response to peritubular sodium removal was accompanied by cell acidification indicating bicarbonate efflux; 4. all aforementioned phenomena were inhibited by SITS (10−3 mol/l) except for a small SITS-independent sodium efflux and depolarization which occurred in response to peritubular sodium removal and was not accompanied by cell pH changes; 5. bicarbonate efflux and accompanying potential changes in response to reduction of peritubular bicarbonate virtually vanished in sodium-free solutions. From these observations we conclude that bicarbonate efflux proceeds as rheogenic sodium-bicarbonate cotransport with a stoichiometry of bicarbonate to sodium greater than 1. The question which of the charged species of the bicarbonate buffer system moves cannot yet be decided. Attempts to determine the stoichiometry from the SITS-inhibitable initial cell depolarization and from the SITS-inhibitable initial fluxes suggest a stoichiometry of 3 HCO 3 − : 1 Na+. In addition to sodium-dependent bicarbonate flux, evidence was obtained for a sodium-independent transport system of acids or bases which is able to regulate cell pH even in sodium-free solutions.
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      headline:Rheogenic sodium-bicarbonate cotransport in the peritubular cell membrane of rat renal proximal tubule
      description:The mechanism of bicarbonate transport across the peritubular cell membrane was investigated in rat kidney proximal tubules in situ by measuring cell pH and cell Na+ activity in response to sudden reduction of peritubular Na+ and/or HCO 3 − . The following observations were made: 1. sudden peritubular reduction of either ion concentration produced the same transient depolarizing potential response; 2. bicarbonate efflux in response to peritubular reduction of bicarbonate was accompanied by sodium efflux; 3. sodium efflux in response to peritubular sodium removal was accompanied by cell acidification indicating bicarbonate efflux; 4. all aforementioned phenomena were inhibited by SITS (10−3 mol/l) except for a small SITS-independent sodium efflux and depolarization which occurred in response to peritubular sodium removal and was not accompanied by cell pH changes; 5. bicarbonate efflux and accompanying potential changes in response to reduction of peritubular bicarbonate virtually vanished in sodium-free solutions. From these observations we conclude that bicarbonate efflux proceeds as rheogenic sodium-bicarbonate cotransport with a stoichiometry of bicarbonate to sodium greater than 1. The question which of the charged species of the bicarbonate buffer system moves cannot yet be decided. Attempts to determine the stoichiometry from the SITS-inhibitable initial cell depolarization and from the SITS-inhibitable initial fluxes suggest a stoichiometry of 3 HCO 3 − : 1 Na+. In addition to sodium-dependent bicarbonate flux, evidence was obtained for a sodium-independent transport system of acids or bases which is able to regulate cell pH even in sodium-free solutions.
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      dateModified:
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         Rheogenic sodium-bicarbonate cotransport
         Stoichiometry
         Sodium-independent cell pH regulation
         Human Physiology
         Molecular Medicine
         Neurosciences
         Cell Biology
         Receptors
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