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Nitric oxide and vasodilation in human limbs

M J Joyner1, N M Dietz

  • 1Department of Anesthesiology, Mayo Clinic and Foundation, Rochester, Minnesota 55905, USA. joyner.michael@mayo.edu

Journal of Applied Physiology (Bethesda, Md. : 1985)
|February 14, 1998
PubMed
Summary

Nitric oxide (NO) plays a varying role in human vasodilation. While not essential for reactive hyperemia or body heating, NO is crucial for mental stress-induced vasodilation and may aid exercise hyperemia.

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Area of Science:

  • Physiology
  • Vascular Biology
  • Human Circulation

Background:

  • Human skin and skeletal muscle exhibit significant vasodilation in response to physiological stimuli like exercise, stress, and heating.
  • The precise mechanisms and signaling molecules responsible for these vasodilation responses remain incompletely understood.
  • Nitric oxide (NO) has emerged as a potential mediator in regulating blood flow to skin and muscle.

Purpose of the Study:

  • To investigate the role of nitric oxide (NO) in mediating vasodilation during various physiological stimuli in human skin and skeletal muscle.
  • To clarify the contribution of NO to reactive hyperemia, exercise hyperemia, mental stress-induced vasodilation, and vasodilation during whole-body heating.
  • To explore potential mechanisms of NO release and its implications in disease states.

Main Methods:

  • The study reviews existing literature and preliminary evidence on nitric oxide's role in human hyperemic responses.
  • Physiological stimuli examined include reactive hyperemia, exercise hyperemia, mental stress, and whole-body heating.
  • Focus is on NO's contribution to vasodilation in cutaneous and skeletal muscle vascular beds.

Main Results:

  • Nitric oxide (NO) is not essential for reactive hyperemia or vasodilation during body heating.
  • NO appears to play a modest role in exercise hyperemia.
  • NO is a major contributor to skeletal muscle vasodilation induced by mental stress.

Conclusions:

  • Nitric oxide (NO) plays a differential role in various human hyperemic responses, being critical for stress-induced vasodilation but less so for others.
  • The exact mechanisms of NO release and its regulation in these vascular beds require further investigation.
  • While NO is a potent vasodilator, it does not solely explain all observed vasodilation, indicating the involvement of other pathways.

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