AJP - Heart and Circulatory Physiology, Vol 250, Issue 3 519-H523, Copyright © 1986 by American Physiological Society
Effect of vibration on a canine cutaneous artery
L. E. Lindblad, R. R. Lorenz, J. T. Shepherd and P. M. Vanhoutte
Vibration of rings of isolated canine saphenous arteries depressed
contractions induced by potassium chloride, prostaglandin F2 alpha, and
activation of the adrenergic nerve endings by electrical stimulation. Peak
contractions to exogenous norepinephrine were not significantly affected by
vibration, being augmented, unchanged, or depressed, whereas contractions
during the stable plateau phase were depressed. The calcium entry blocker
diltiazem reduced the peak response but not the stable plateau phase of the
contraction to norepinephrine; in the presence of diltiazem, vibration
still depressed the latter. When vibration was applied during the steady
state of contractions evoked by electrical stimulation, the depression was
immediate, and its extent increased with both the amplitude (0.025-0.10 mm)
and the frequency (30-150 Hz) of vibration. In arteries labeled with
[3H]norepinephrine, vibration (120 Hz, 0.1 mm amplitude) during electrical
stimulation induced a slight but significant increase in the release of
labeled transmitter. It is suggested that the depression of contractions to
potassium ions, prostaglandin F2 alpha, sympathetic nerve stimulation, and
the plateau phase of the response to exogenous norepinephrine are caused by
vibration depressing the force-generating process in vascular smooth
muscle. Failure of vibration to significantly depress the peak contraction
to norepinephrine may be explained by the facilitation by vibration of the
influx of extracellular calcium ions.
