Effect of the Ca(2+)-channel agonist Bay K 8644 on the contractile responses in human placental veins.

Journal of autonomic pharmacology Pub Date : 1996-06-01
M T Barrús, J Reviriego, J Marín
{"title":"Effect of the Ca(2+)-channel agonist Bay K 8644 on the contractile responses in human placental veins.","authors":"M T Barrús,&nbsp;J Reviriego,&nbsp;J Marín","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>1. The aim of the present study was to analyse, in segments of human placental veins, the effect of the Ca2+ channel agonist Bay K 8644 (0.1 microM) and Ca2+ channel antagonists nifedipine (0.1 microM) and diltiazem (1 microM) on vascular contractility and 45Ca2+ uptake. 2. The Ca2+ channel agonist Bay K 8644 (0.1 microM) caused small concentration dependent contractions that were increased by a moderate membrane depolarization with 7.5 mM K+. This increase was reversed by nifedipine and diltiazem. Ca2+ addition to segments previously depolarized with 75 mM K+ and exposed to a Ca(2+)-free medium caused contractile responses that were increased by 0.1 microM Bay K 8644; such an increase was blocked by 0.1 microM nifedipine and 1 microM diltiazem. 3. K+ and 5-HT induced concentration dependent contractile responses which were increased by Bay K 8644 (0.1 microM). Both 0.1 microM nifedipine and 1 microM diltiazem inhibited the increasing effect of Bay K 8644. Bay K 8644 (30 nM and 0.1 microM) caused an enhancement in 45Ca2+ accumulation over the basal value, that was increased by membrane depolarization with K+ (7.5, 15 and 30 nM) and inhibited by nifedipine (0.1 microM). K+ (15 and 30, but not 7.5 mM) and 5-HT (1 microM) induced 45Ca2+ uptake over the basal level that was increased by Bay K 8644 (0.1 microM). Such an increase was antagonized by nifedipine (0.1 microM). 4. These data indicate that: (1) a small depolarization with K+ is needed for Bay K 8644 to be able to produce consistent contractile responses, suggesting that voltage gated Ca2+ channels (VGCCs) are not activated in a basal situation in placental veins; (2) the increase of 5-HT contraction by Bay K 8644 may be produced by either the capability of this amine to depolarize the membrane of smooth muscle cells and subsequent facilitation of Ca2+ influx through VGCCs or direct activation by Bay K 8644 of receptor (5-HT) operated Ca2+ channels (ROCs), and (3) the increasing effect of Bay K 8644 appears to be due to a Ca2+ entry activation through VGCCs.</p>","PeriodicalId":15103,"journal":{"name":"Journal of autonomic pharmacology","volume":"16 3","pages":"161-7"},"PeriodicalIF":0.0000,"publicationDate":"1996-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of autonomic pharmacology","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

1. The aim of the present study was to analyse, in segments of human placental veins, the effect of the Ca2+ channel agonist Bay K 8644 (0.1 microM) and Ca2+ channel antagonists nifedipine (0.1 microM) and diltiazem (1 microM) on vascular contractility and 45Ca2+ uptake. 2. The Ca2+ channel agonist Bay K 8644 (0.1 microM) caused small concentration dependent contractions that were increased by a moderate membrane depolarization with 7.5 mM K+. This increase was reversed by nifedipine and diltiazem. Ca2+ addition to segments previously depolarized with 75 mM K+ and exposed to a Ca(2+)-free medium caused contractile responses that were increased by 0.1 microM Bay K 8644; such an increase was blocked by 0.1 microM nifedipine and 1 microM diltiazem. 3. K+ and 5-HT induced concentration dependent contractile responses which were increased by Bay K 8644 (0.1 microM). Both 0.1 microM nifedipine and 1 microM diltiazem inhibited the increasing effect of Bay K 8644. Bay K 8644 (30 nM and 0.1 microM) caused an enhancement in 45Ca2+ accumulation over the basal value, that was increased by membrane depolarization with K+ (7.5, 15 and 30 nM) and inhibited by nifedipine (0.1 microM). K+ (15 and 30, but not 7.5 mM) and 5-HT (1 microM) induced 45Ca2+ uptake over the basal level that was increased by Bay K 8644 (0.1 microM). Such an increase was antagonized by nifedipine (0.1 microM). 4. These data indicate that: (1) a small depolarization with K+ is needed for Bay K 8644 to be able to produce consistent contractile responses, suggesting that voltage gated Ca2+ channels (VGCCs) are not activated in a basal situation in placental veins; (2) the increase of 5-HT contraction by Bay K 8644 may be produced by either the capability of this amine to depolarize the membrane of smooth muscle cells and subsequent facilitation of Ca2+ influx through VGCCs or direct activation by Bay K 8644 of receptor (5-HT) operated Ca2+ channels (ROCs), and (3) the increasing effect of Bay K 8644 appears to be due to a Ca2+ entry activation through VGCCs.

Ca(2+)通道激动剂Bay k8644对人胎盘静脉收缩反应的影响
1. 本研究的目的是分析,在人类胎盘静脉段,Ca2+通道激动剂Bay K 8644(0.1微米)和Ca2+通道拮抗剂硝苯地平(0.1微米)和地尔硫卓(1微米)对血管收缩性和45Ca2+吸收的影响。2. Ca2+通道激动剂Bay K 8644(0.1微米)引起小的浓度依赖性收缩,并通过7.5毫米K+适度的膜去极化而增加。硝苯地平和地尔硫卓逆转了这种增加。Ca2+加入到先前用75 mM K+去极化的片段中,暴露于无Ca(2+)的介质中,导致收缩反应增加0.1 microM Bay K 8644;0.1 μ m硝苯地平和1 μ m地尔硫卓阻断了这种增加。3.K+和5-HT诱导了浓度依赖性的收缩反应,Bay K 8644 (0.1 μ m)增强了收缩反应。0.1 μ m硝苯地平和1 μ m地尔硫卓均抑制了Bay k8644的增殖作用。Bay K 8644 (30 nM和0.1 microM)使45Ca2+的积累高于基础值,K+(7.5、15和30 nM)使45Ca2+的积累增加,硝苯地平(0.1 microM)抑制45Ca2+的积累。K+(15和30,但不是7.5 mM)和5-HT(1微米)诱导45Ca2+摄取超过基础水平,Bay K 8644(0.1微米)增加。硝苯地平(0.1微米)可拮抗这种增加。4. 这些数据表明:(1)Bay K 8644需要少量的K+去极化才能产生一致的收缩反应,这表明在胎盘静脉的基础情况下,电压门控Ca2+通道(VGCCs)没有被激活;(2) Bay K 8644增加5-HT收缩可能是由于该胺能够使平滑肌细胞膜去极化并随后通过VGCCs促进Ca2+内流,或者Bay K 8644直接激活受体(5-HT)操作的Ca2+通道(ROCs)。(3)Bay K 8644增加的效果似乎是由于Ca2+通过VGCCs进入激活。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信