Intact rat superior mesenteric artery endothelium is an electrical syncytium and expresses strong inward rectifier K+ conductance

Background and purposeVascular endothelial and smooth muscle cell phenotypes may change dramatically after isolation and in cell cultures. This study was designed to investigate gap junctions coupling in an integrated intact preparation and to test if KIR channels modulate resting membrane conductance in “in situ” endothelial cells (EC), and acetylcholine (ACh)-evoked relaxation of the rat superior mesenteric artery.Experimental approachWhole cell blind patch recordings of ionic currents from in situ EC, dye-coupling experiments, and functional studies were performed in rat superior mesenteric artery.Key resultsEC were dye-coupled through gap junctions. 18β-glycyrretinic acid (25 μM) decreased outward and inward currents, the 80% decay of time and time constant of the capacitative transients, capacitance, and increased input resistance. Barium chloride (30 μM) decreased resting and ACh-evoked inward currents, the sensitivity of ACh-evoked relaxation, and decreased both the sensitivity and the maximal relaxation to S-nitroso-N-acetyl penicillamine in arteries with, but not in arteries without endothelium.ConclusionsThe present results suggest that the EC layer of this large artery is electrically coupled, and that KIR channels regulate resting inward conductance, hence suggesting that they are of importance for resting membrane potential in in situ EC. Moreover, EC KIR channels are involved in ACh-evoked relaxation.

► This experimental approach allows studying gap junctions coupling in an integrated intact preparation by means of in situ patch clamp.
► The endothelial layer of a large artery, besides resistance arteries, is also an electrical syncitium.
► Inward ionic conductance in intact endothelial cells is mediated by inward rectifying channels.