Prostaglandin E2 stimulation of oxygen consumption in parietal cells and of H+ transport in gastric mucosa of the rat.

Physiological chemistry and physics Pub Date : 1982-01-01
T J Sernka, J E Caplan
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Abstract

Since prostaglandin E2 is generally stimulatory to intestinal and nonparietal gastric secretions, possible stimulation of parietal gastric acid secretion was investigated. Oxygen consumption of parietal cells isolated from rat stomach was determined before and after addition of 16,16-dimethyl prostaglandin E2 (dmPGE2). At low concentration, dmPGE2 significantly stimulated oxygen consumption of parietal cells by 7%. Concomitantly, acid secretion rose. H+ transport in the isolated gastric mucosa of the rat was determined in the absence of electrochemical gradients to preclude H+ back-diffusion. Compared with control rates, H+ transport from submucosal to mucosal side was stimulated 51% by the same low concentration of dmPGE2. It is concluded that stimulation of gastric acid secretion by parietal cells appears to be a physiological function of prostaglandin E2 in the stomach. The results support the hypothesis that prostaglandins stimulate secretory responses throughout the gastrointestinal tract.

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前列腺素E2对大鼠胃壁细胞耗氧及胃粘膜H+转运的影响。
由于前列腺素E2通常刺激肠道和非胃壁分泌物,因此研究了可能刺激胃壁酸分泌的可能性。测定大鼠胃壁细胞在添加16,16-二甲基前列腺素E2 (dmPGE2)前后的耗氧量。低浓度时,dmPGE2显著刺激壁细胞耗氧量7%。与此同时,胃酸分泌也增加了。在没有电化学梯度阻止H+反扩散的情况下,测定了大鼠离体胃粘膜中H+的转运。与对照组相比,同样低浓度的dmPGE2刺激了51%的H+从粘膜下到粘膜侧的转运。由此可见,胃壁细胞刺激胃酸分泌可能是胃中前列腺素E2的一种生理功能。结果支持前列腺素刺激整个胃肠道分泌反应的假设。
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