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

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 microM) failed to stimulate any significant accumulation of IP3 during the 5 min period following its application. In the presence of prazosin, 5-HT (300 microM) 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 microM) 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 alpha 1-adrenoceptor antagonist, prazosin (0.1 microM). 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.