Acute vibration increases 2C-adrenergic smooth muscle constriction and alters thermosensitivity of cutaneous arteries

Krajnak, K., R. G. Dong, S. Flavahan, D. Welcome, and N. A. Flavahan. Acute vibration increases 2C-adrenergic smooth muscle constriction and alters thermosensitivity of cutaneous arteries. J Appl Physiol 100: 1230–1237, 2006. First published December 8, 2005; doi:10.1152/japplphysiol.00761.2005.—The vascular symptoms of hand-arm vibration syndrome, including cold-induced vasospasm, are in part mediated by increased sensitivity of cutaneous arteries to sympathetic stimulation. The goal of the present study was to use a rat tail model to analyze the effects of vibration on vascular function and -adrenoceptor (AR) responsiveness. Rats were exposed to a single period of vibration (4 h, 125 Hz, constant acceleration 49 m/s root mean square). The physical or biodynamic response of the tail demonstrated increased transmissibility or resonance at this frequency, similar to that observed during vibration of human fingers. Morphological analysis demonstrated that vibration did not appear to cause structural injury to vascular cells. In vitro analysis of vascular function demonstrated that constriction to the 1-AR agonist phenylephrine was similar in vibrated and control arteries. In contrast, constriction to the 2-AR agonist UK14304 was increased in vibrated compared with control arteries, both in endothelium-containing or endothelium-denuded arteries. The 2C-AR antagonist MK912 (3 10 10 M) inhibited constriction to UK14304 in vibrated but not control arteries, reversing the vibration-induced increase in 2-AR activity. Moderate cooling (to 28°C) increased constriction to the 2-AR agonist in control and vibrated arteries, but the magnitude of the amplification was less in vibrated compared with control arteries. Endothelium-dependent relaxation to acetylcholine was similar in control and vibrated arteries. Based on these results, we conclude that a single exposure to vibration caused a persistent increase in 2C-ARmediated vasoconstriction, which may contribute to the pathogenesis of vibration-induced vascular disease.