The study concerned Ca2+ channels that are receptor-operated by norepinephrine (NE) and mediate hyper-reactivity of vas deferens smooth muscle from rats with streptozotocin (STZ)-induced diabetes, and the mediatory responses of these channels, such as tension development, Ca2+ uptake and phosphatidylinositol (PI) turnover. The contractile responses induced by adrenoceptor agonists were significantly greater in diabetic rat vas deferens than in the controls. A greater Ca2+ uptake was induced by 10(-5) M NE in strips from diabetic rats than in the controls. The uptake of Ca2+ was completely inhibited by 10(-6) M prazosin but not by 10(-5) M verapamil. Enhancement of Ca2+ release by 10(-5) M NE was faster and greater in diabetic muscles than in the controls. The accumulation of [3H]inositol phosphates was increased 4-fold in the controls and 7-fold in diabetic muscles by 10(-5) M NE. This increase was completely inhibited by 10(-6) M prazosin but not by 10(-6) M yohimbine. The data suggest that vas deferens smooth muscle hyper-reactivity in diabetic rats is due to increased PI turnover mediated by alpha 1-adrenoceptors, to the release of intracellular bound Ca2+ and to an increase of Ca2+ uptake through receptor-operated Ca2+ channels.

译文

该研究涉及由去甲肾上腺素 (NE) 受体操作的Ca2通道,并介导链脲佐菌素 (STZ) 诱导的糖尿病大鼠输精管平滑肌的高反应性,以及这些通道的介导反应,例如紧张发展,ca2 + 摄取和磷脂酰肌醇 (PI) 更新。糖尿病大鼠输精管中肾上腺素受体激动剂诱导的收缩反应明显大于对照组。与对照组相比,糖尿病大鼠的10(-5) M NE诱导的Ca2摄取更大。10(-6) M哌唑嗪完全抑制了Ca2的吸收,但没有抑制10(-5) M维拉帕米。与对照组相比,糖尿病肌肉中10(-5) M NE增强Ca2释放的速度更快且更大。10(-5) M NE在对照组中 [3H] 肌醇磷酸盐的积累增加了4倍,在糖尿病肌肉中增加了7倍。这种增加被10(-6) M哌唑嗪完全抑制,但没有被10(-6) M育亨宾抑制。数据表明糖尿病大鼠输精管平滑肌高反应性是由于 α1-肾上腺素受体介导的PI转换增加,通过受体操作的Ca2通道释放细胞内结合的Ca2并增加Ca2的摄取。

+1
+2
100研值 100研值 ¥99课程
检索文献一次
下载文献一次

去下载>

成功解锁2个技能,为你点赞

《SCI写作十大必备语法》
解决你的SCI语法难题!

技能熟练度+1

视频课《玩转文献检索》
让你成为检索达人!

恭喜完成新手挑战

手机微信扫一扫,添加好友领取

免费领《Endnote文献管理工具+教程》

微信扫码, 免费领取

手机登录

获取验证码
登录