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.