首页> 美国卫生研究院文献>Biochemical Journal >Increase in pituitary adenosine 3′:5′-cyclic monophosphate content and potentiation of growth-hormone release from heifer anterior pituitary slices incubated in the presence of 3-isobutyl-1-methylxanthine
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Increase in pituitary adenosine 3′:5′-cyclic monophosphate content and potentiation of growth-hormone release from heifer anterior pituitary slices incubated in the presence of 3-isobutyl-1-methylxanthine

机译:在3-异丁基-1-甲基黄嘌呤存在下孵育的垂体小母牛垂体前叶片中垂体腺苷3:5-环一磷酸含量的增加和生长激素释放的增强

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摘要

The release of growth hormone from heifer anterior pituitary slices and the cyclic AMP content of the slices were increased by the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine, both increases being related to inhibitor concentration over the range 0.1–1.0mm. Neither Ba2+ (6.9 or 2.3mm), K+ (72mm), nor p-chloromercuribenzoate (20μm) had any effect on pituitary cyclic AMP content over a 20min period. 3-Isobutyl-1-methylxanthine potentiated the release of growth hormone in response to Ba2+ (2.3mm) and K+ (24mm), but the degree of potentiation did not depend on inhibitor concentration in the same way as did tissue cyclic AMP content. 3-Isobutyl-1-methylxanthine decreased the concentration of K+ required to give maximum stimulation of growth-hormone release, but did not significantly increase the maximum response to Ba2+. Growth-hormone release in the presence of prostaglandin E2 (1μm) was increased by 3-isobutyl-1-methylxanthine and was inhibited by the prostaglandin antagonist, 7-oxa-13-prostynoic acid, although this antagonist increased the pituitary cyclic AMP concentration and potentiated the prostaglandin E2-induced rise in cyclic AMP content. The stimulation of growth-hormone release by p-chloromercuribenzoate was not potentiated by 3-isobutyl-1-methylxanthine. The data suggest that Ba+ and K+ act at the same point in the secretory process as 3-isobutyl-1-methylxanthine, although by a different mechanism, and that p-chloromercuribenzoate has a different point of action.
机译:磷酸二酯酶抑制剂3-异丁基-1-甲基黄嘌呤增加了小母牛垂体前叶切片中生长激素的释放和切片中环AMP的含量,两者的增加均与抑制剂浓度在0.1-1.0mm范围内有关。在20分钟内,Ba 2 + (6.9或2.3mm),K + (72mm)和对氯汞苯甲酸(20μm)均不影响垂体循环AMP含量。 。 3-异丁基-1-甲基黄嘌呤增强了对Ba 2 + (2.3mm)和K + (24mm)的生长激素的释放,但增强程度确实与组织循环AMP含量相同,它并不取决于抑制剂的浓度。 3-异丁基-1-甲基黄嘌呤降低了最大程度地刺激生长激素释放所需的K + 的浓度,但并未显着增加对Ba 2 + 的最大反应。 3-异丁基-1-甲基黄嘌呤增加前列腺素E2(1μm)存在时生长激素的释放,并被前列腺素拮抗剂7-oxa-13-炔雌酸抑制,尽管该拮抗剂增加了垂体环AMP的浓度和增强了前列腺素E2诱导的循环AMP含量的上升。对氯mercuribenzoate刺激生长激素释放没有被3-异丁基-1-甲基黄嘌呤增强。数据表明,Ba + 和K + 在分泌过程中的作用与3-异丁基-1-甲基黄嘌呤相同,尽管机理不同。 -氯巯基苯甲酸具有不同的作用点。

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