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1 Department of Human Biology and Nutritional Sciences, University of Guelph, Guelph, Ontario, Canada N1G 1J6; and 2 Department of Pharmacology and Physiology, University of Rochester, Rochester, New York 14642
To
determine whether nitric oxide (NO), adenosine (Ado) receptors, or
ATP-sensitive potassium (KATP) channels play a role in
arteriolar dilations induced by muscle contraction, we used a cremaster
preparation in anesthetesized hamsters in which we stimulated four to
five muscle fibers lying perpendicular to a transverse arteriole
(maximal diameter ~35-65 µm). The diameter of the arteriole at
the site of overlap of the stimulated muscle fibers (the local site)
and at a remote site ~1,000 µm upstream (the upstream site) was
measured before, during, and after muscle contraction. Two minutes of
4-Hz muscle stimulation (5-15 V, 0.4 ms) produced local and
upstream dilations of 19 ± 1 and 10 ± 1 µm, respectively.
N
-nitro-L-arginine
(10
4 M; NO synthase inhibitor), xanthine amine congener
(XAC; 106 M; Ado A1, A2A, and
A2B receptor antagonist), or glibenclamide (Glib;
105 M; KATP channel inhibitor) superfused
over the preparation attenuated the local dilation (by 29.7 ± 12.7, 61.8 ± 9.0, and 51.9 ± 14.9%, respectively), but
only XAC and Glib attenuated the upstream dilation (by 68.9 ± 6.8 and 89.1 ± 6.4%, respectively). Furthermore, only Glib, when
applied to the upstream site directly, attenuated the upstream dilation
(48.1 ± 9.1%). Neither XAC nor Glib applied directly to the
arteriole between the local and the upstream sites had an effect on the
magnitude of the upstream dilation. We conclude that NO, Ado receptors,
and KATP channels are involved in the local dilation
initiated by contracting muscle and that both KATP channels
and Ado receptor stimulation, but not NO, play a role in the
manifestation of the dilation at the upstream site.
microvasculature; adenosine; nitric oxide; adenosine 5'-triphosphate-sensitive potassium channels; metabolic control of blood flow
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