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 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.