Mechanism of luminal alkalinization by bullfrog fundic mucosa

K. Takeuchi, A. Merhav, W. Silen

Research output: Contribution to journalArticlepeer-review

Abstract

Metiamide-inhibited fundic mucosa of bullfrog secreted alkali (OH-) at 0.1-0.2 μeq.cm-2.h-1.OH- was abolished by dinitrophenol (DNP) and was decreased significantly by 4,4-didsothiocyano-2,2-disulfonate stilbene (DIDS), anoxia, or HCO3 --free nutrient solution in Na+ solutions, increasing nutrient, [HCO3 -] augmented OH- and I(sc) linearly while resistance (R) decreased. No such changes occurred in Na+-free nutrient solution. In all experiments, ΔI(sc) was ~12 x ΔOH. Replacement of Cl- in the secretory solutions or in the nutrient solutions had no significant influence on OH-. When Na+-free nutrient solutions and Cl--free secretory solutions were present, OH- decreased significantly (P < 0.01). Increasing nutrient [Cl-] in the absence of secretory Cl- significantly (P < 0.01) augmented OH- and I(sc). In the absence of secretory Cl-. OH- and I(sc) were linearly related to varying nutrient [Cl-]. In tissues with nutrient solutions on the secretory side and vice versa, apparent OH- was 0.4-0.5 μeq.cm-2.h-1 and was dependent on secretory [HCO3 -] but was affected by DNP, DIDS, or replacement of Cl- on secretory or nutrient solutions. We conclude that 1) OH- secretion is dependent on nutrient HCO3 - and Na+ and oxidative metabolism, 2) endogenous HCO3 - does not contribute significantly, and 3) adequate tissue Cl- must be present for normal OH-.

Original languageEnglish
JournalAmerican Journal of Physiology - Gastrointestinal and Liver Physiology
Volume6
Issue number5
Publication statusPublished - 1982

ASJC Scopus subject areas

  • Physiology
  • Gastroenterology

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