{"title":"Specific accumulation of inositol 1,4,5-trisphosphate in rabbit basilar artery in response to noradrenaline but not 5-hydroxytryptamine","authors":"Timothy V. Murphy , Christopher J. Garland","doi":"10.1016/0922-4106(95)90026-8","DOIUrl":null,"url":null,"abstract":"<div><p>This study examined the ability of 5-hydroxytryptamine and noradrenaline to stimulate inositol 1,4,5-trisphosphate (IP<sub>3</sub>) mass accumulation in segments of the rabbit basilar artery. 5-Hydroxytryptamine (5-HT, 100 ωM) failed to stimulate any significant accumulation of IP<sub>3</sub> during the 5 min period following its application. In the presence of prazosin, 5-HT (300 ωM) caused a rapid, transient decrease in IP<sub>3</sub> 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 IP<sub>3</sub> 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<sup>+</sup> (normal concentration 5.7 mM), the basal IP<sub>3</sub> concentration was significantly elevated. The IP<sub>3</sub> accumulation stimulated by either 5-HT or raised K<sup>+</sup> was not reduced by the presence of the α<sub>1</sub>-adrenoceptor antagonist, prazosin (0.1 ωM). In the presence of raised K<sup>+</sup>, 5-hydroxytryptamine caused a rapid, transient inhibition of the K<sup>+</sup>-induced IP<sub>3</sub> 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 IP<sub>3</sub> accumulation induced by raised extracellular [K<sup>+</sup>]. These results provide further evidence that IP<sub>3</sub> 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.</p></div>","PeriodicalId":100502,"journal":{"name":"European Journal of Pharmacology: Molecular Pharmacology","volume":"290 2","pages":"Pages 141-144"},"PeriodicalIF":0.0000,"publicationDate":"1995-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0922-4106(95)90026-8","citationCount":"2","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"European Journal of Pharmacology: Molecular Pharmacology","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/0922410695900268","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
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.