Prostaglandin E2-histamine in interactions on cAMP, cGMP, and acid production in isolated fundic glands.
Prostaglandin E2-histamine in interactions on cAMP, cGMP, and acid production in isolated fundic glands.
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前列腺素 E2-组胺对离体胃底腺中 cAMP、cGMP 和酸产生的相互作用。
DOI：
10.1152/ajpgi.1982.242.1.g21
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发表时间：
1982
期刊：
影响因子：
--
通讯作者：
C. Ramsay
中科院分区：
文献类型：
--
作者：
R. Levine;K. R. Kohen;E. Schwartzel;C. Ramsay
在离体兔胃底粘膜腺体中研究了cAMP、cGMP、产酸量[用[14 C]氨基比林（AP）的腺内蓄积量测定]和前列腺素E2（PGE 2）活性之间的关系。AP，cAMP和cGMP对组胺，PGE 2和3-异丁基-1-甲基黄嘌呤（IMX）的反应与对照组进行了比较。组胺和前列腺素E2显着增加腺体cAMP水平的两倍，组胺和IMX刺激AP摄取2至4倍。PGE 2显着抑制组胺和IMX刺激的AP积累，但它没有改变基础AP摄取。PGE 2也降低组胺刺激的cAMP产生，但仅在低浓度（10（-7）M）下。该剂量的PGE 2接近未刺激腺体中发现的内源性PGE 2含量（10（-8）M）。未刺激腺体中的腺内cGMP水平（10（-8）M）。腺内cGMP水平增加IMX，但不是由前列腺素E2或组胺。它的结论是，组胺刺激酸分泌是由cAMP介导的，组胺的分泌和生化反应由前列腺素E2调制，因为前列腺素E2拮抗组胺刺激的cAMP和AP的摄取，并在cAMP的上升，仅由前列腺素E2诱导似乎是本地化的nonparalyetal细胞，因为PGE 2单独不刺激AP的积累。
Relations among cAMP, cGMP, acid production [measured by the intraglandular accumulation of [14C]aminopyrine (AP)], and prostaglandin E2 (PGE2) activity were studied in isolated glands from rabbit fundic mucosa. AP, cAMP, and cGMP responses to histamine, PGE2, and 3-isobutyl-1-methylxanthine (IMX) were compared with controls. Histamine and PGE2 significantly increased glandular cAMP levels twofold, and histamine and IMX stimulated AP uptake two- to fourfold. PGE2 significantly inhibited both histamine- and IMX-stimulated AP accumulation, but it did not alter basal AP uptake. PGE2 also decreased histamine-stimulated cAMP production but only at a low concentration (10(-7) M). This dose of PGE2 was near to the endogenous PGE2 content found in unstimulated glands (10(-8) M). Intraglandular cGMP levels in unstimulated glands (10(-8) M). Intraglandular cGMP levels were increased by IMX but not by PGE2 or histamine. It is concluded that histamine stimulation of acid secretion is mediated by cAMP, that secretory and biochemical responses to histamine are modulated by PGE2 because PGE2 antagonized histamine-stimulated cAMP and AP uptake, and that the rise in cAMP induced solely by PGE2 appears to be localized within nonparietal cells because PGE2 alone did not stimulate AP accumulation.