Calcium antagonists and hormone release. II. Effects of verapamil on basal, gonadotropin-releasing hormone- and thyrotropin-releasing hormone-induced pituitary hormone release in normal subjects.
Calcium antagonists and hormone release. II. Effects of verapamil on basal, gonadotropin-releasing hormone- and thyrotropin-releasing hormone-induced pituitary hormone release in normal subjects.
复制标题
钙拮抗剂和激素释放。
DOI：
10.1210/jcem-51-4-749
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发表时间：
1980
期刊：
影响因子：
--
通讯作者：
L. De Marinis
中科院分区：
文献类型：
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作者：
A. Barbarino;L. De Marinis
虽然已经确定Ca2+在几种激素的释放中起重要作用，但对垂体激素释放过程中Ca2+与促分泌物之间的相互作用知之甚少。研究下丘脑释放激素的作用机制可能的途径之一是研究有机钙拮抗剂对其作用的影响。因此，我们将常用的钙拮抗剂维拉帕米输注到20名正常受试者（10男10女，年龄19-37岁）体内，研究其对垂体基底激素水平的影响以及促性腺激素释放激素（GnRH）和TRH诱导的激素释放增强的影响。维拉帕米以5mg /h的速率输注3小时，在男性和女性中诱导了循环LH和FSH水平的显著抑制。在输注结束时，LH（60%）对释放的抑制大于FSH（54%）。终止输注后，血浆促性腺激素浓度在2小时内逐渐恢复到基础水平。维拉帕米也能够减弱促性腺激素对GnRH的峰值增量反应。尽管基础TSH浓度明显不受维拉帕米的影响，但在男性和女性中，TRH对TSH的增量反应均被显著抑制。维拉帕米输注既不影响基础PRL浓度也不影响PRL对TRH的反应。我们的数据证明维拉帕米对正常受试者垂体激素的释放有不同的影响。它抑制中枢和外周介导的促性腺激素释放，并减弱TSH对TRH的反应。相反，维拉帕米似乎不影响基础或trh介导的PRl释放。有机钙拮抗剂在体外和体内实验模型中的应用，似乎为进一步研究促分泌剂在激素释放过程中的作用机制提供了一个有前途的工具。
Although it has been well established that Ca2+ plays an essential role in the release of several hormones, very little is known of the interactions between Ca2+ and secretagogues in the process of pituitary hormone release. One possible way of studying the mechanism of action of hypothalamic releasing hormones is to study how organic calcium antagonists affect their action. Consequently, we infused the commonly used calcium antagonist, verapamil, into 20 normal subjects (10 men and 10 women; aged 19-37 yr) and studied its effects on both basal pituitary hormone levels and augmented hormonal release induced by gonadotropin-releasing hormone (GnRH) and TRH. Verapamil, infused at a rate of 5 mg/h for 3 h, induced a significant and marked suppression of circulating LH and FSH levels in both men and women. By the end of the infusion, the suppression of release was greater for LH (60%) than for FSH (54%). After the termination of the infusion, plasma gonadotropin concentrations returned progressively to basal levels within 2 h. Verapamil was also capable of blunting the peak incremental gonadotropin response to GnRH. Although the basal TSH concentration was apparently unaffected by verapamil, the incremental TSH response to TRH was significantly inhibited in both men and women. Verapamil infusion did not affect either the basal PRL concentration or the PRL response to TRH. Our data provide evidence that verapamil exerts different effects on the release of pituitary hormones in normal subjects. It inhibits the centrally mediated as well as the peripherally mediated gonadotropin release and blunts the TSH response to TRH. On the contrary, verapamil does not seem to affect basal or TRH-mediated PRl release. The use of organic calcium antagonists in experimental models in vitro as well as in vivo appears to offer a promising tool for further studies on the mechanism of action of secretagogues in the process of hormone release.