The contractile behaviour of gastrointestinal smooth muscles is dependent on the intrinsic electrical activities of the muscles.1 Depolarisation activates L-type Ca²⁺channels that provide the main pathway for Ca²⁺ to enter gastrointestinal smooth muscle cells. This is particularly true for the phasic portions of the gastrointestinal tract where cyclic depolarisations and repolarisations, referred to as slow waves, set the contractile frequency and maintain the phasic nature of contractions (fig 1). The slow wave cycle ensures a period of relaxation between contractions, allowing mixing and movement of luminal contents. Tonic regions of the gastrointestinal tract, such as the sphincters, are also regulated by electrical events but primarily by more persistent changes in resting membrane potential.

In addition to the ionic conductances that contribute to resting membrane potential and electrical rhythmicity, there are several ionic conductances that are modulated by neural and hormonal inputs. Regulatory inputs from nerves, hormones, and paracrine substances are superimposed on the spontaneous electrical activity of gastrointestinal muscles. Electrical responses to biologically active substances result from: (i) modulation of ionic conductances that are already active and going through dynamic changes in open probability during the slow wave cycle; and (ii) activation of agonist dependent conductances that do not participate in basal electrical activity. Ca²⁺ entry into smooth muscles is mainly controlled by rather subtle changes in the open probability of L-type Ca²⁺channels.2 3 The more frequently these channels open and the longer they stay open, …