Effect of Amino Acids on H⁺ Production by Isolated Rat Parietal Cells

Abstract

We investigated the hypothesis of a direct effect of amino acids on gastric parietal cells. [¹⁴C]aminopyrine uptake into isolated enriched rat parietal cells served as a quantitative index of H⁺ production. Cells were incubated in media containing 1 mM Ca²⁺ in the absence or presence of the phosphodiesterase inhibitor 3-isobutyl-l-methylxanthine (IBMX), or 3 mM Ca²⁺ without IBMX. Under these different conditions, L-arginine, L-phenylalanine and L-tryptophan (10^-6M to 3 × 10^-2M) failed to alter basal [¹⁴C]aminopyrine uptake as well as the response to submaximal stimulation by histamine, forskolin, N⁶O²-dibutyryladenosine-3´,5´-(cyclic)-phosphate (db cAMP) or carbachol. Pentagastrin failed to elicit an appreciable response in the presence and absence of 10^-3 M of all three amino acids studied. It is concluded that in vivo the potent stimulation of gastric acid secretion by L-arginine, L-phenylalanine and L-tryptophan is mediated by other than direct mechanisms.

The role of gastric histamine release in the acid secretory response to pentagastrin and methacholine in the dog

“…Gastrin and cholinergic agonists stimulate the release of histamine from the rat stomach, and gastrin is a potent inducer of the enzyme, histidine decarboxylase, the rate limiting enzyme in the synthesis of histamine [6,8,22,23]. The rat parietal cell is unresponsive to gastrin [24], and in the isolated vascularly perfused rat stomach, the amount of histamine that is released to gastrin can explain the acid secretory response to that secretagogue [8]. The interaction between cholinergic stimulation and histamine release is less conclusive even in the rodent model of acid secretion [6, 221. The other hypothesis, known as the permission hypothesis, is based on work in the canine model of acid secretion.…”