Specific accumulation of inositol 1,4,5-trisphosphate in rabbit basilar artery in response to noradrenaline but not 5-hydroxytryptamine

Timothy V. Murphy , Christopher J. Garland
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引用次数: 2

Abstract

This study examined the ability of 5-hydroxytryptamine and noradrenaline to stimulate inositol 1,4,5-trisphosphate (IP3) mass accumulation in segments of the rabbit basilar artery. 5-Hydroxytryptamine (5-HT, 100 ωM) failed to stimulate any significant accumulation of IP3 during the 5 min period following its application. In the presence of prazosin, 5-HT (300 ωM) caused a rapid, transient decrease in IP3 accumulation which was significant after 5 s but had increased to pre-stimulation levels within 15 s. In contrast, noradrenaline (10 ωM) stimulated a rapid, transient accumulation of IP3 which was significant after 5 s but had declined to basal levels after 60 s. In basilar artery segments bathed in Krebs solution containing 25.7 mM K+ (normal concentration 5.7 mM), the basal IP3 concentration was significantly elevated. The IP3 accumulation stimulated by either 5-HT or raised K+ was not reduced by the presence of the α1-adrenoceptor antagonist, prazosin (0.1 ωM). In the presence of raised K+, 5-hydroxytryptamine caused a rapid, transient inhibition of the K+-induced IP3 accumulation, which was maximal after 5 s but had increased to pre-stimulation levels within 30 s in the continued presence of 5-hydroxytryptamine. Noradrenaline did not affect the IP3 accumulation induced by raised extracellular [K+]. These results provide further evidence that IP3 is not involved in 5-hydroxytryptamine-induced smooth muscle contraction in the rabbit basilar artery, but support a role for this second messenger in the contraction induced in response to noradrenaline.

肌醇1,4,5-三磷酸在兔基底动脉对去甲肾上腺素而非5-羟色胺的特异性积累
本研究检测了5-羟色胺和去甲肾上腺素刺激兔基底动脉段肌醇1,4,5-三磷酸(IP3)堆积的能力。5-羟色胺(5- ht, 100 ωM)在施用后的5分钟内未能刺激IP3的显著积累。在prazosin存在的情况下,5- ht (300 ωM)在5 s后引起IP3积累的快速、短暂的下降,但在15 s内增加到刺激前的水平。相反,去甲肾上腺素(10 ωM)刺激IP3快速、短暂积累,在5 s后显著,但在60 s后下降到基础水平。在含有25.7 mM K+(正常浓度5.7 mM)的Krebs溶液中,基底动脉段IP3浓度显著升高。α1-肾上腺素能受体拮抗剂prazosin (0.1 ωM)的存在不会降低5-HT或K+升高刺激的IP3积累。在K+升高的情况下,5-羟色胺对K+诱导的IP3积累产生快速、短暂的抑制作用,在5 s后达到最大,但在5-羟色胺持续存在的情况下,IP3积累在30 s内增加到刺激前的水平。去甲肾上腺素不影响细胞外[K+]升高引起的IP3积累。这些结果进一步证明IP3不参与5-羟色胺诱导的兔基底动脉平滑肌收缩,但支持IP3在去甲肾上腺素诱导的收缩中所起的作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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