Vascular and neural mechanisms of ACh-mediated vasodilation in the forearm cutaneous microcirculation

被引:103
作者
Berghoff, M
Kathpal, M
Kilo, S
Hilz, MJ
Freeman, R
机构
[1] Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med, Dept Neurol,Autonom & Peripheral Nerve Lab, Boston, MA 02215 USA
[2] Univ Erlangen Nurnberg, Dept Neurol, D-91054 Erlangen, Germany
关键词
endothelium; prostaglandin; nitric oxide; axon reflex; acetylcholine;
D O I
10.1152/japplphysiol.01167.2000
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
The relative contribution of endothelial vasodilating factors to acetylcholine (ACh) mediated vasodilation in the forearm cutaneous microcirculation is unclear. The aims of this study were to investigate the contributions of prostanoids and cutaneous C fibers to basal cutaneous blood flow (CuBF) and ACh-mediated vasodilation. ACh was iontophoresed into the forearm, and cutaneous perfusion was measured by laser-Doppler flowmetry. To inhibit the production of prostanoids, four doses of acetylsalicylic acid (ASA; 81, 648, 972, and 1,944 mg) were administered orally. Cutaneous nerve fibers were blocked with topical anesthesia. Cyclooxygenase inhibition did not change basal CuBF or endothelium-mediated vasodilation to ACh. In contrast, ASA (972 and 1,944 mg) significantly reduced the C-fiber-mediated axon reflex in a dose-dependent fashion. Blockade of C-fiber function significantly reduced axon reflex-mediated vasodilation but did not affect basal CuBF or endothelium-dependent vasodilation. The findings suggest that prostanoids do not contribute significantly to basal CuBF or endothelium-dependent vasodilation in the forearm microcirculation. In contrast, prostanoids are mediators of the ACh-provoked axon reflex.
引用
收藏
页码:780 / 788
页数:9
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