Scheme showing the Ca2+ mediated processes involved in α1-adrenoceptor stimulation of mouse aortic segments with PE.
PE causes phasic Ca2+ increase and concomitant contraction by releasing Ca2+ from the SR (event 1). This is accompanied by influx of Ca2+ via complex interactions between NSCC and VGCC and the steady-state contraction by PE is determined by the relative contribution of window Ca2+ influx via VGCC (very voltage-dependent) and Ca2+ influx via NSCC (less voltage-dependent) (event 2). Window VGCC Ca2 influx and related contraction are inhibited by diltiazem, membrane potential repolarization with K+ or levcromakalim and Ca2+ release from non-contractile Ca2+ stores by CPA and stimulated by high K+ and BAY K844 (event 3). NSCC Ca2 influx and related contraction are inhibited by 2-APB and very high K+ (strong depolarization to −20 mV or less negative) and stimulated by Ca2+ release from non-contractile Ca2+ stores with CPA (event 4). CPA causes high Ca2+ release from a non-contractile compartment of the SR (event 5). Emptying of the non-contractile Ca2+ store with CPA causes large Ca2+ influx, which is accompanied with minor contraction in the absence of PE, but which turns the PE-induced contraction to one that is mainly mediated by NSCC. This points to a complex interaction between the non-contractile and contractile SR Ca2+ stores and their refilling via VGCC and/or different NSCC.