Nitric oxide inhibits cutaneous vasoconstriction to exogenous norepinephrine

Manabu Shibasaki, David A. Low, Scott L. Davis, Craig G. Crandall

Research output: Contribution to journalArticle

38 Citations (Scopus)

Abstract

Previously, we found that nitric oxide (NO) inhibits cutaneous vasoconstrictor responsiveness evoked by whole body cooling, as well as an orthostatic stress in the heat-stressed human (Shibasaki M, Durand S, Davis SL, Cui J, Low DA, Keller DM, Crandall CG. J Physiol 585: 627-634, 2007). However, it remains unknown whether this response occurs via NO acting through presynaptic or postsynaptic mechanisms. The aim of this study was to test the hypothesis that NO is capable of impairing cutaneous vasoconstriction via postsynaptic mechanisms. Skin blood flow was monitored over two forearm sites where intradermal microdialysis membranes were previously placed. Skin blood flow was elevated four- to fivefold through perfusion of the NO donor sodium nitroprusside at one site and through perfusion of adenosine (primarily non-NO mechanisms) at a second site. Once a plateau in vasodilation was evident, increasing concentrations of norepinephrine (1 × 10-8 to 1 × 10-2 M) were administrated through both microdialysis probes, while the aforementioned vasodilator agents continued to be perfused. Cutaneous vascular conductance was calculated by dividing skin blood flow by mean arterial blood pressure. The administration of norepinephrine decreased cutaneous vascular conductance at both sites. However, the dose of norepinephrine at the onset of vasoconstriction (-5.9 ± 1.3 vs. -7.2 ± 0.7 log M norepinephrine, P = 0.021) and the concentration of norepinephrine resulting in 50% of the maximal vasoconstrictor response (-4.9 ± 1.2 vs. -6.1 ± 0.2 log M norepinephrine dose; P = 0.012) occurred at significantly higher norepinephrine concentrations for the sodium nitroprusside site relative to the adenosine site, respectively. These results suggested that NO is capable of attenuating cutaneous vasoconstrictor responsiveness to norepinephrine via postsynaptic mechanisms.

Original languageEnglish (US)
Pages (from-to)1504-1508
Number of pages5
JournalJournal of Applied Physiology
Volume105
Issue number5
DOIs
StatePublished - Nov 2008

Fingerprint

Vasoconstriction
Norepinephrine
Nitric Oxide
Skin
Vasoconstrictor Agents
Microdialysis
Nitroprusside
Adenosine
Blood Vessels
Arterial Pressure
Perfusion
Nitric Oxide Donors
Vasodilator Agents
Forearm
Vasodilation
Oxides
Hot Temperature
Membranes

Keywords

  • Cutaneous vasoconstrictor responsiveness
  • Endogenous norepinephrine
  • Norepinephrine dose-response curve

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

Cite this

Nitric oxide inhibits cutaneous vasoconstriction to exogenous norepinephrine. / Shibasaki, Manabu; Low, David A.; Davis, Scott L.; Crandall, Craig G.

In: Journal of Applied Physiology, Vol. 105, No. 5, 11.2008, p. 1504-1508.

Research output: Contribution to journalArticle

Shibasaki, Manabu ; Low, David A. ; Davis, Scott L. ; Crandall, Craig G. / Nitric oxide inhibits cutaneous vasoconstriction to exogenous norepinephrine. In: Journal of Applied Physiology. 2008 ; Vol. 105, No. 5. pp. 1504-1508.
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