Integrative Physiology |
From The John B. Pierce Laboratory and the Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, Conn.
Correspondence to Steven S. Segal, PhD, John B. Pierce Laboratory, Yale University School of Medicine, 290 Congress Ave, New Haven, CT 06519. E-mail sssegal{at}jbpierce.org
AbstractAcetylcholine
(ACh) evokes the conduction of vasodilation along resistance
microvessels. However, it is not known which cell layer
(endothelium or smooth muscle) serves as the conduction
pathway. In isolated, cannulated feed arteries (
70 µm in
diameter at 75 mm Hg; length
4 mm) of the hamster
retractor muscle, we tested the hypothesis that
endothelial cells provide the pathway for conduction.
Microiontophoresis of ACh (500 ms, 500 nA) onto the distal end of a
feed artery evoked hyperpolarization (-13±2 mV)
of both cell layers with vasodilation (15±1 µm) along the
entire vessel. To selectively damage endothelial cells
(confirmed by loss of vasodilation to ACh and labeling of disrupted
cells with propidium iodide), an air bubble was perfused through a
portion of the vessel lumen, or a 70-kDa
fluorescein-conjugated dextran (FCD) was illuminated within
a segment (300 µm) of the lumen. After
endothelial cell damage,
hyperpolarization and vasodilation conducted up to,
but not through, the treated segment. To selectively damage smooth
muscle cells (confirmed by loss of vasoconstriction to
phenylephrine and labeling with propidium iodide), FCD was
perifused around the vessel and illuminated. Vasodilation and
hyperpolarization conducted past the disrupted
smooth muscle cells without attenuation. We conclude that
endothelial cells provide the pathway for conducting
hyperpolarization and vasodilation along feed
arteries in response to ACh.
Key Words: feed artery conduction endothelium hyperpolarization vasodilation
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