Vasoactive intestinal peptide treatment that increases thyroid blood flow fails to alter plasma T3 or T4 levels in the rat.

Vasoactive intestinal peptide treatment that increases thyroid blood flow fails to alter plasma T3 or T4 levels in the rat.
复制标题

增加甲状腺血流量的血管活性肠肽治疗无法改变大鼠血浆 T3 或 T4 水平。

DOI:
10.1159/000124970
复制
发表时间:
1988
期刊:
影响因子:
4.1
通讯作者:
Hedge,GA
Hedge,GA
中科院分区:
医学2区
文献类型:
--
作者:
Huffman,LJ;Connors,JM;White,BH;Hedge,GA

文献摘要

被引文献

相似文献

含有血管活性肠肽(VIP)的神经纤维撞击甲状腺中的滤泡细胞和血管。我们以前已经表明,VIP诱导一个特定的,剂量相关的增加甲状腺血流量在大鼠。然而,我们的VIP治疗对循环甲状腺激素水平没有影响。由于一些报告表明,VIP可以增强甲状腺激素分泌,我们已经扩大了我们的研究,以更完整地描述条件下,VIP可能刺激大鼠甲状腺激素分泌。在未麻醉、无应激的长期导管大鼠中,33 µg VIP/100 g体重未能改变三碘甲状腺原氨酸(TO)或甲状腺素(T4)水平,也未影响甲状腺对次最大剂量牛TSH的分泌反应。在甲状腺功能正常和甲状腺功能亢进的大鼠中,外源性TSH可增加125 I的释放,而VIP对125 I的释放无影响。我们观察到循环T3水平响应VIP升高的唯一条件是在连续2小时输注高剂量(0.25 µg/min,i. v.)这种肽。然而,这些大鼠的血浆TSH水平往往升高,表明通过TSH的间接影响。我们观察到,VIP在体内局部应用(0.1 μg/μl,持续3小时)或体外处理(10- 6 M,持续4小时)后,不能改变T3或T4的释放,尽管这些制剂对牛TSH完全有反应,但这一结果进一步证实了上述观点。尽管缺乏甲状腺激素分泌反应,VIP刺激环AMP释放在体外,表明至少有一些组成部分的甲状腺是响应于这种肽。因此,虽然VIP似乎可以引起甲状腺激素分泌,但只有在远远超过调节甲状腺血流的治疗条件下才能观察到这种作用。这使我们相信,甲状腺VIP在甲状腺激素分泌的正常生理调节中几乎没有重要性。
Vasoactive-intestinal-peptide (VΙP)-containing nerve fibers impinge upon both follicle cells and blood vessels in the thyroid gland. We have previously shown that VIP induces a specific, dose-related increase in thyroid blood flow in the rat. However, our VIP treatments had no effect on circulating thyroid hormone levels. Since a number of reports have indicated that VIP can enhance thyroid hormone secretion, we have expanded our studies to characterize more completely the conditions under which VIP might stimulate thyroid hormone secretion in the rat. In unanesthetized, unstressed rats with chronic catheters, 33 µg VIP/100 g body weight failed to alter triiodothyronine (TO or thyroxine (T4) levels and did not affect the thyroid secretory response to a submaximal dose of bovine TSH. In euthyroid and hyperthyroid rats, the release of125I was increased after exogenous TSH, but was not altered by VIP. The only condition in which we observed a rise in circulating T3 levels in response to VIP was during a continuous 2 h infusion of a high dose (0.25 µg/min, i.v.) of this peptide. However, plasma TSH levels tended to be elevated in these rats, suggesting an indirect effect via TSH. This suggestion is strengthened by our observation that VIP failed to alter T3or T4release after topical application (0.1 µg/µl for 3 h) in vivo or after in vitro treatment (10–6Mfor 4 h), even though these preparations were fully responsive to bovine TSH. Despite the lack of a thyroid hormone secretory response, VIP did stimulate cyclic AMP release in vitro, indicating that at least some component of the thyroid is responsive to this peptide. Thus, while it appears that VIP can elicit thyroid hormone secretion, such effects are observed only under treatment conditions which greatly exceed those shown to modulate thyroid blood flow. This leads us to believe that thyroidal VIP has little or no importance in the normal physiological regulation of thyroid hormone secretion.