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The John B. Pierce Laboratory and Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, Connecticut 06519
We performed intracellular recording with
Lucifer yellow dye microinjection to investigate the cellular
pathway(s) by which constriction and dilation are conducted along the
wall of arterioles (diameter 47 ± 1 µm,
n = 63) supplying blood flow to the
cheek pouch of anesthetized hamsters. At rest, membrane potential
(Em) of
endothelial (
36 ± 1 mV) and smooth muscle (35 ± 1 mV) cells was not different. Micropipette delivery of norepinephrine
(NE) or phenylephrine (PE) produced smooth muscle cell depolarization (5-41 mV) and vasoconstriction (7-49 µm) at the site of
release and along the arteriole with no effect on
Em of endothelial
cells. KCl produced conduction of depolarization and
vasoconstriction with similar electrical kinetics in endothelial and
smooth muscle cells. Acetylcholine triggered conduction of vasodilation
(2-25 µm) and hyperpolarization (3-33 mV) along both cell
layers; in smooth muscle, this change in
Em was prolonged
and followed by a transient depolarization. These cell-specific
electrophysiological recordings uniquely illustrate that depolarization
and constriction are initiated and conducted along smooth muscle,
independent of the endothelium. Furthermore, conduction of vasodilation
is explained by the spread of hyperpolarization along homologously
coupled endothelial and smooth muscle cells, with distinctive responses between cell layers. The discontinuity between endothelium and smooth
muscle indicates that these respective pathways are not electrically
coupled during blood flow control.
gap junctions; blood flow control; cell-to-cell communication; cell coupling; membrane potential; endothelium-derived hyperpolarizing factor; microcirculation; resistance vessels
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