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From the John B. Pierce Laboratory and Departments of Epidemiology and Public Health and of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, Conn.
Correspondence to Steven S. Segal, PhD, The John B. Pierce Laboratory, Yale University School of Medicine, 290 Congress Ave, New Haven, CT 06519.
Abstract We tested the hypothesis that sympathetic nerve
activity can influence the conduction of vasodilation along the
arteriolar wall. Arterioles in the superfused cremaster muscle of
anesthetized male hamsters (n=21, 109±4 g) were studied.
Microelectrodes were positioned adjacent to the distal end of primary
arterioles to stimulate sympathetic nerves throughout arteriolar
networks (perivascular nerve stimulation [PNS]). Microiontophoresis
micropipettes (tip outer diameter, 1 to 2 µm) filled with
acetylcholine (ACh, 1 mol/L) were positioned adjacent to the wall of
second-order (2A) or third-order (3A) arterioles
1 mm distal to
their origin to induce local and conducted vasodilation; diameter
responses were recorded at the micropipette tip and at vessel origins,
respectively. For 2A and 3A arterioles (resting diameters, 15 to 54 and
9 to 30 µm, respectively), vasoconstriction with PNS was frequency
dependent (0.5 to 32 Hz); this was attenuated by 65%
(P<.05) with
-adrenoceptor blockade (phentolamine, 1
µmol/L). Conducted vasodilation was attenuated by >40% during 16-Hz
PNS (P<.05); this effect was reversed by
phentolamine. In a reciprocal fashion, conducted vasodilation
diminished PNS-induced vasoconstriction by
50% (P<.05).
Elevating oxygen (from 0% to 10%) in the superfusion solution induced
vasoconstriction similar to that with 16-Hz PNS yet had no effect on
conduction. Neural blockade with tetrodotoxin (1 µmol/L) eliminated
PNS-induced vasoconstriction and enhanced (P<.05) conducted
vasodilation. These findings indicate that perivascular nerves in
striated muscle can influence cell-to-cell communication along the
arteriolar wall both at rest and during enhanced sympathetic activity.
The attenuation of sympathetic vasoconstriction by conducted
vasodilation suggests a novel explanation for functional sympatholysis.
Key Words: microcirculation perivascular nerve stimulation microiontophoresis acetylcholine adrenoceptors
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