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1 The John B. Pierce Laboratory and Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, Connecticut 06519; and 2 Department of Human Physiology, Flinders University of South Australia, Adelaide 5001, South Australia
The conduction of vasodilation
along resistance vessels has been presumed to reflect the electrotonic
spread of hyperpolarization from cell to cell along the vessel wall
through gap junction channels. However, the vasomotor response to
acetylcholine (ACh) encompasses greater distances than can be explained
by passive decay. To investigate the underlying mechanism for this
behavior, we tested the hypothesis that ACh augments the conduction of
hyperpolarization. Feed arteries (n = 23; diameter,
58 ± 4 µm; segment length, 2-8 mm) were isolated from the
hamster retractor muscle, cannulated at each end, and pressurized to 75 mmHg (at 37°C). Vessels were impaled with one or two dye-containing
microelectrodes simultaneously (separation distance, 50 µm to 3.5 mm). Membrane potential (Em) (rest,
approximately 
30 mV) and electrical responses were similar between
endothelium and smooth muscle, as predicted for robust myoendothelial
coupling. Current injection (0.8 nA, 1.5 s) evoked
hyperpolarization (10 ± 1 mV; membrane time constant, 240 ms)
that conducted along the vessel with a length constant (
) = 1.2 ± 0.1 mm; spontaneous Em oscillations
(~1 Hz) decayed with = 1.2 + 0.1 mm. In contrast, ACh
microiontophoresis (500 nA, 500 ms, 1 µm tip) evoked
hyperpolarization (14 ± 2 mV) that conducted with = 1.9 ± 0.1 mm, 60% further (P < 0.05) than
responses evoked by purely electrical stimuli. These findings indicate
that ACh augments the conduction of hyperpolarization along the vessel wall.
cable theory; length constant; microcirculation; endothelium; smooth muscle
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