Smooth muscle gap-junctions allow propagation of intercellular Ca waves and vasoconstriction due to Ca based action potentials in rat mesenteric resistance arteries.

The role of vascular gap junctions in the conduction of intercellular Ca and vasoconstriction along small resistance arteries is not entirely understood. Some depolarizing agents trigger conducted vasoconstriction while others only evoke a local depolarization. Here we use a novel technique to investigate the temporal and spatial relationship between intercellular Ca signals generated by smooth muscle action potentials (APs) and vasoconstriction in mesenteric resistance arteries (MA). Pulses of exogenous KCl to depolarize the downstream end (T1) of a 3 mm long artery increased intracellular Ca associated with vasoconstriction. The spatial spread and amplitude of both depended on the duration of the pulse, with only a restricted non-conducting vasoconstriction to a 1 s pulse. While blocking smooth muscle cell (SMC) K channels with TEA and activating L-type voltage-gated Ca channels (VGCCs) with BayK 8644 spread was dramatically facilitated, so the 1 s pulse evoked intercellular Ca waves and vasoconstriction that spread along an entire artery segment 3000 μm long. Ca waves spread as nifedipine-sensitive Ca spikes due to SMC action potentials, and evoked vasoconstriction. Both intercellular Ca and vasoconstriction spread at circa 3 mm s and were independent of the endothelium. The spread but not the generation of Ca spikes was reversibly blocked by the gap junction inhibitor 18β-GA. Thus, smooth muscle gap junctions enable depolarization to spread along resistance arteries, and once regenerative Ca-based APs occur, spread along the entire length of an artery followed by widespread vasoconstriction.