ABSTRACT

Functional evidence suggests that myoendothelial gap junctions in the rat mesenteric artery may facilitate the spread of current from hyperpolarized endothelial cells to adjacent smooth muscle cells. Morphological evidence supports this heterocellular coupling, and in addition, the possibility for homocellular coupling. The present study investigated the extent to which hyperpolarization of smooth muscle cells can spread along the longitudinal axis of mesenteric arteries. Membrane potential was measured with glass microelectrodes in smooth muscle. Either acetylcholine or levcromakalim were focally pressure-ejected from glass pipettes to a small segment of artery. Both direct and indirect hyperpolarization of smooth muscle cells evoked similar conducted responses (to over 2mm upstream), and the conducted response was markedly reduced in arteries without endothelium. The injection of propidium iodide into either endothelial or smooth muscle cells indicated both homo-and heterocellular coupling, but the spread was more effective between the endothelial cells. These data indicate that the hyperpolarization of smooth muscle, stimulated either by endothelium-derived hyperpolarizing factor or directly with agonists, spreads longitudinally along the axis of the artery, and this spread is facilitated by the endothelium.