Regulation of gastric somatostatin secretion in the mouse by luminal acidity: a local feedback mechanism.
Regulation of gastric somatostatin secretion in the mouse by luminal acidity: a local feedback mechanism.
复制标题
通过管腔酸度调节小鼠胃生长抑素分泌：局部反馈机制。
DOI：
10.1016/0016-5085(88)90418-0
复制
发表时间：
1988
期刊：
影响因子：
29.4
通讯作者：
Makhlouf,GM
中科院分区：
文献类型：
--
作者：
Schubert,ML;Edwards,NF;Makhlouf,GM
本研究旨在确定组胺或五肽胃泌素诱导的小鼠离体胃的生长抑素分泌是分泌物对胃生长抑素细胞的直接作用，还是由胃腔酸度增加所介导的间接作用。外源性酸(80-480nmol/min)灌流可引起生长抑素分泌增加，与管腔酸度增加成正比。生长抑素分泌的增加对河豚毒素具有抵抗力，并达到最大水平(61.6%±8.7%)，与最大剂量促分泌剂的作用相似。相反，用碳酸氢钠(20-160nmol/min)中和基础酸的分泌会导致生长抑素分泌的减少，与腔酸度的降低成比例。类似地，用碳酸氢钠中和促分泌剂诱导的酸分泌增加或用西咪替丁抑制增加的酸分泌取消了相应的生长抑素分泌增加。有人认为，酸诱导的生长抑素在壁细胞附近的释放是一种抑制酸分泌的负反馈机制。
The present study was designed to determine whether somatostatin secretion induced by histamine or pentagastrin in the isolated luminally perfused mouse stomach was a direct effect of the secretagogues on gastric somatostatin cells or an indirect effect mediated by the increase in luminal acidity. Perfusion of the lumen with exogenous acid (80–480 nmol/min) caused an increase in somatostatin secretion in proportion to the increase in luminal acidity. The increase in somatostatin secretion was resistant to tetrodotoxin and attained maximal levels (61.6% ± 8.7% above basal level) similar to those elicited by maximal doses of secretagogues. Conversely, neutralization of basal acid secretion with bicarbonate (20–160 nmol/min) caused a decrease in somatostatin secretion in proportion to the decrease in luminal acidity. Similarly, neutralization of the secretagogue-induced increments in acid secretion with bicarbonate or inhibition of the increments with cimetidine abolished the corresponding increments in somatostatin secretion. It is proposed that acid-induced release of somatostatin in proximity to parietal cells serves as a negative feedback mechanism restraining acid secretion.