Schepp W, Heim H K, Ruoff H J
Agents Actions. 1983 Apr;13(2-3):200-6. doi: 10.1007/BF01967331.
In isolated rat gastric cells somatostatin and PGE2 were compared in respect to their effects on the cAMP system and on the histamine-stimulated H+-production, measured by 14C-aminopyrine (14C-AP) uptake. Like PGE2 somatostatin activated adenylate cyclase (AC) for all in non-parietal cells. This effect on AC declined in cell fractions with increasing number of parietal cells. Activation of AC or elevation of cellular cAMP and uptake of 14C-AP in response to histamine were inhibited by 10(-9) to 10(-5) mol/1 PGE2 and somatostatin. The results indicate remarkable similarity between somatostatin and PGE2: both activate a non-parietal cell AC and both inhibit H+-production, likely by interfering at the histamine sensitive AC of the parietal cell.
在分离的大鼠胃细胞中,比较了生长抑素和前列腺素E2(PGE2)对环磷酸腺苷(cAMP)系统以及对组胺刺激的氢离子(H⁺)产生的影响,后者通过¹⁴C - 氨基比林(¹⁴C - AP)摄取来测量。与PGE2一样,生长抑素在所有非壁细胞中均激活腺苷酸环化酶(AC)。随着壁细胞数量增加,这种对AC的作用在细胞组分中减弱。10⁻⁹至10⁻⁵ mol/1的PGE2和生长抑素抑制了AC的激活或细胞内cAMP的升高以及对组胺的¹⁴C - AP摄取。结果表明生长抑素和PGE2之间存在显著相似性:两者均激活非壁细胞AC,并且两者均可能通过干扰壁细胞的组胺敏感AC来抑制H⁺产生。