Multiple dilator pathways in skeletal muscle contraction-induced arteriolar dilations

• Published in: American journal of physiology. Regulatory, integrative and comparative physiology integrative and comparative physiology, 2002-04, Vol.282 (4), p.969-R978
• Main Authors: Murrant, Coral L, Sarelius, Ingrid H
• Format: Article
• Language: English
• Subjects: Adenosine - metabolism; Adenosine Triphosphate - metabolism; Animals; Anti-Arrhythmia Agents - pharmacology; Arterioles - physiology; Cricetinae; Enzyme Inhibitors - pharmacology; Glyburide - pharmacology; Male; Mesocricetus; Muscle Contraction - physiology; Muscle, Skeletal - blood supply; Muscle, Skeletal - physiology; Nitric Oxide - metabolism; Nitroarginine - pharmacology; Potassium Channels - metabolism; Receptors, Purinergic P1 - metabolism; Vasodilation - drug effects; Vasodilation - physiology; Xanthines - pharmacology
• ISSN: 0363-6119; 1522-1490
• DOI: 10.1152/ajpregu.00405.2001

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 (K ATP ) 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; 10 6 M; Ado A 1 , A 2A , and A 2B receptor antagonist), or glibenclamide (Glib; 10 5 M; K ATP 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 K ATP channels are involved in the local dilation initiated by contracting muscle and that both K ATP 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