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Vol. 83, Issue 6, 1785-1796, December 1997
Department of Anesthesiology, Mayo Clinic and Foundation, Rochester, Minnesota 55905
Joyner, Michael J., and Niki M. Dietz.
Nitric oxide and vasodilation in human limbs. J. Appl. Physiol. 83(6): 1785-1796, 1997.
Both the
skeletal muscle and skin of humans possess remarkable abilities to
vasodilate. Marked vasodilation can be seen in these vascular beds in
response to a variety of common physiological stimuli. These stimuli
include reactive hyperemia (skin and muscle), exercise hyperemia
(muscle), mental stress (muscle), and whole body heating (skin). The
physiological mechanisms that cause vasodilation in response to these
stimuli are poorly understood, and the substance(s) responsible for it
remain unclear. In this context, recent attention has been focused on
the possible contribution of nitric oxide (NO) to the regulation of
hyperemic responses in human skin and skeletal muscle. The emerging
picture is that NO is not an essential component of the dilator
response seen during reactive hyperemia. However, it does appear that
NO may play a modest role in exercise hyperemia. NO appears to play a
major role in the skeletal muscle vasodilation seen in response to
mental stress in humans. Preliminary evidence also indicates that NO is
not essential for the normal dilator responses observed in the
cutaneous circulation during body heating in humans, but this issue
needs further study. There are a number of possible mechanisms that
might mediate NO release in humans, and the role of these mechanisms in
the various hyperemic responses is also poorly understood. The role of
altered NO-mediated vasodilation in some disease states is also
discussed. Whereas NO is a potent vasodilating substance, the actions
of NO alone do not explain a variety of poorly understood vasodilator
mechanisms in conscious humans. Much work remains for those interested
in the role of NO in the regulation of blood flow to the skin and skeletal muscle of humans.
muscle blood flow; skin blood flow; exercise; reactive hyperemia; endothelium
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