ATP dependence of H+ secretion.
Cells in isolated rabbit gastric gland were made permeable to ATP by high voltage discharge across a gland suspension. In both normal (5.4 mM K+) and high K+ (108 mM) medium, this electrical shock resulted in a marked reduction in the ability of the parietal cell to produce and accumulate acid. Acid production was monitored both microscopically by acridine orange accumulation in the secretory canaliculus and by accumulation of the weak base [14C]aminopyrine. In 108 mM K+ solutions but not in 5.4 mM K+ solutions 5, mM ATP was able to restore the accumulation of these probes to control (unshocked) levels. When shocked glands had been previously stimulated by secretagogues, the aminopyrine accumulation ratio was only partly restored by ATP. Inhibition of mitochondrial respiration by cyanide, azide, or Amytal abolished acid secretion; the subsequent addition of ATP to shocked glands increased the aminopyrine accumulation ratio to 47 and resulted in an acridine orange fluorescence indistinguishable from that of histamine-stimulated, unshocked glands. We conclude that ATP can act as a substrate for H+ secretion in the parietal cell, and that perhaps no additional energy source is necessary.
D000255:Adenosine Triphosphate / Q000494:pharmacology*; D000632:Aminopyrine / Q000378:metabolism; D000818:Animals; D002118:Calcium / Q000494:pharmacology; D003486:Cyanides / Q000494:pharmacology; D005088:Exocrine Glands / Q000187:drug effects / Q000378:metabolism*; D005750:Gastric Juice / Q000378:metabolism*; D005753:Gastric Mucosa / Q000378:metabolism*; D007700:Kinetics; D008928:Mitochondria / Q000378:metabolism; D008954:Models, Biological; D011188:Potassium / Q000494:pharmacology; D011817:Rabbits
D003486:Cyanides; D000632:Aminopyrine; D000255:Adenosine Triphosphate; D011188:Potassium; D002118:Calcium