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Department of Pharmacology and Physiology, University of Rochester School of Medicine and Dentistry, Rochester, New York 14642
In
hamster cremaster muscle, it has been shown previously that contraction
of skeletal muscle fibers underlying small groups of capillaries
(modules) induces dilations that are proportional to metabolic rate in
the two arteriolar generations upstream of the stimulated capillaries
(Berg BR, Cohen KD, and Sarelius IH. Am J Physiol Heart Circ
Physiol 272: H2693-H2700, 1997). These remote dilations were hypothesized to be transmitted via gap junctions and not perivascular nerves. In the present study, halothane (0.07%) blocked dilation in the module inflow arteriole, and dilation in the
second arteriolar generation upstream, the branch arteriole, was
blocked by both 600 mosM sucrose and halothane but not tetrodotoxin (2 µM). Dilations in both arterioles were not blocked by the gap junction uncoupler 18-
-glycyrrhetinic acid (40 µM), and 80 mM KCl
did not block dilation of the module inflow arteriole. These data
implicate a gap junctional-mediated pathway insensitive to 18-
-glycyrrhetinic acid in dilating the two arterioles upstream of
the capillary module during "remote" muscle contraction. Dilation in the branch arteriole, but not the module inflow arteriole, was
attenuated by 100 µM
N
-nitro-L-arginine. Thus selective
contraction of muscle fibers underneath capillaries results in
dilations in the upstream arterioles that have characteristics
consistent with a signal that is transmitted along the vessel wall
through gap junctions, i.e., a conducted vasodilation. The observed
insensitivities to 18-
-glycyrrhetinic acid, to KCl, and to
N
-nitro-L-arginine suggest, however,
that there are multiple signaling pathways by which remote dilations
can be initiated in these microvessels.
microcirculation; cell signaling; conducted dilation; gap junctions
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