Increased 45Ca influx in response to alpha 1-adrenoceptor stimulation in spontaneously hypertensive rat caudal artery.

Increased 45Ca influx in response to alpha 1-adrenoceptor stimulation in spontaneously hypertensive rat caudal artery.
复制标题

自发性高血压大鼠尾动脉中 α1-肾上腺素受体刺激导致 45Ca 流入增加。

DOI:
10.1097/00005344-198708000-00011
复制
发表时间:
1987
影响因子:
3
通讯作者:
Bhalla,RC
Bhalla,RC
中科院分区:
医学4区
文献类型:
--
作者:
Aqel,MB;Sharma,RV;Bhalla,RC

文献摘要

相似文献

本文观察了自发性高血压大鼠(SHR)和Wistar京都正常血压大鼠(WKY)尾动脉对去甲肾上腺素(NE)和甲氧胺刺激的等长张力发展和~(45)Ca内流的反应。与WKY相比,SHR尾动脉对NE和甲氧胺刺激所产生的最大等长张力和45Ca内流均显著增加(p<0.05)。另一方面,WKY和SHR尾动脉对K+去极化的反应所产生的等长张力和4,Ca内流均无差异。对分离的WKY和SHR尾动脉膜[~3H]哌唑嗪结合的测定表明,SHR 128+/-14 PM和WKY 141+/-19 PM的Kd值为单一的高亲和力结合部位,SHR 108+/-14fmol/mg蛋白和WKY 113+/-21fmol/mg蛋白的BMA为108fmol/mg蛋白。根据这些结果,我们得出结论:(A)SHR尾动脉环对[α],-肾上腺素受体刺激的收缩反应增强,至少部分是由于通过受体操作的Ca:+通道增加了钙内流;(B)[~3H]哌唑嗪结合所估计的[α]-肾上腺素受体的亲和力或密度在SHR尾动脉中没有改变。
The isometric tension development and 45Ca influx in response to norepinephrine (NE) and methox-amine stimulation were investigated in caudal arteries of spontaneously hypertensive rats (SHR) and Wistar Kyoto normotensive rats (WKY). The maximum isometric tension developed as well as 45Ca influx in response to NE and methoxamine stimulation were significantly increased (p< 0.05) in SHR caudal arteries as compared with WKY. On the other hand, neither the isometric tension developed nor the 4, Ca influx in response to K+ depolarization were different between WKY and SHR caudal arteries. Estimation of [3H] prazosin binding to the membranes isolated from caudal artery of WKY and SHR showed a single class of high-affinity binding sites with Kd values for SHR 128+/-14 pM and for WKY 141+/-19 pM, and Bma, values for SHR 108+/-14 fmol/mg protein and for WKY 113+/-21 fmol/mg protein. From these results, we conclude:(a) Increased contractile response of SHR caudal artery rings to [alpha],-adrenoceptor stimulation appears at least in part to be due to an increased Ca2+ influx through receptor-operated Ca:+ channels;(b) the affinity or density of [alpha]-adrenoceptors estimated by [3H] prazosin binding is not altered in the SHR caudal artery.