ENDOTHELIAL AND SMOOTH-MUSCLE CELL CONDUCTION IN ARTERIOLES CONTROLLING BLOOD-FLOW

We performed intracellular recording with Lucifer yellow dye microinje ction to investigate the cellular pathway(s) by which constriction and dilation are conducted along the wall of arterioles (diameter 47 +/- 1 mu m, n = 63) supplying blood flow to the cheek pouch of anesthetize d hamsters. At rest, membrane potential (E-m) of endothelial (-36 +/- 1 mV) and smooth muscle (-35 +/- 1 mV) cells was not different. Microp ipette delivery of norepinephrine (NE) or phenylephrine (PE) produced smooth muscle cell depolarization (5-41 mV) and vasoconstriction (7-49 mu m) at the site of release and along the arteriole with no effect o n E-m of endothelial cells. KCl produced conduction of depolarization and vasoconstriction with similar electrical kinetics in endothelial a nd smooth muscle cells. Acetylcholine triggered conduction of vasodila tion (2-25 mu m) and hyperpolarization (3-33 mV) along both cell layer s; in smooth muscle, this change in E-m was prolonged and followed by a transient depolarization. These cell-specific electrophysiological r ecordings uniquely illustrate that depolarization and constriction are initiated and conducted along smooth muscle, independent of the endot helium. Furthermore, conduction of vasodilation is explained by the sp read of hyperpolarization along homologously coupled endothelial and s mooth muscle cells, with distinctive responses between cell layers. Th e discontinuity between endothelium and smooth muscle indicates that t hese respective pathways are not electrically coupled during blood flo w control.