Acetylcholine-induced vasodilation is mediated by nitric oxide and prostaglandins in human skin.

@article{Kellogg2005AcetylcholineinducedVI,
  title={Acetylcholine-induced vasodilation is mediated by nitric oxide and prostaglandins in human skin.},
  author={D L Kellogg and J. L. Zhao and U. Coey and J Green},
  journal={Journal of applied physiology},
  year={2005},
  volume={98 2},
  pages={
          629-32
        }
}
Acetylcholine (ACh) can effect vasodilation by several mechanisms, including activation of endothelial nitric oxide (NO) synthase and prostaglandin (PG) production. In human skin, exogenous ACh increases both skin blood flow (SkBF) and bioavailable NO levels, but the relative increase is much greater in SkBF than NO. This led us to speculate ACh may dilate cutaneous blood vessels through PGs, as well as NO. To test this hypothesis, we performed a study in 11 healthy people. We measured SkBF by… 

Figures from this paper

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The data suggest that cutaneous acetylcholine‐mediated endothelium‐dependent vasodilation is highly NO‐dependent and is also strongly related to the interactions of NO with prostaglandins.

The effect of nitric oxide synthase and cyclooxygenase inhibition on cutaneous microvascular reactivity

Findings indicate that NO- and PGI2-independent mechanism plays an important role in the regulation of blood flow in the human skin microcirculation.

Cyclooxygenase and nitric oxide synthase dependence of cutaneous reactive hyperemia in humans.

The results suggest that COX inhibition unmasks NO dependence of reactive hyperemia in human cutaneous circulation.

Role of nitric oxide in methacholine-induced sweating and vasodilation in human skin.

It is indicated that nitric oxide acts to augment MCh-stimulated sweat gland function in human skin and that the role of L-NAME in attenuating acetylcholine-induced vasodilation may be due to its potential to act as a muscarinic-receptor antagonist.

Endothelial-derived hyperpolarization contributes to acetylcholine-mediated vasodilation in human skin in a dose-dependent manner.

Cutaneous acetylcholine-mediated dilation is commonly used to assess microvascular function, but the mechanisms of dilation are poorly understood and the roles of endothelial-derived hyperpolarizing factors (EDHFs) are unclear.

Endothelial nitric oxide synthase control mechanisms in the cutaneous vasculature of humans in vivo.

It is concluded that eNOS is predominantly responsible for NO generation in skin during responses to increased T(loc), but not during reflex responses to whole body heat stress.

Cyclooxygenase inhibition does not alter methacholine-induced sweating.

It is shown that both NO synthase and COX inhibition do not influence cholinergic sweating induced by 1-2,000 mM methacholine, and forearm sweating from baseline up to the maximal dose of methACHoline was not different between the four sites.

Roles of nitric oxide synthase isoforms in cutaneous vasodilation induced by local warming of the skin and whole body heat stress in humans.

In forearm skin, eNOS mediates the vasodilator response to increased Tloc and nNOS mediation of the vasodermal response to heat stress, and the two isoforms do not appear to interact during either response.

Inhibition of nitric oxide synthase attenuates cutaneous vasodilation during warm moxibustion-like thermal stimulation in humans.

It is demonstrated that NO is involved in the mechanism of cutaneous vasodilation induced by WMTS, and increases in CVC despite inhibition of the COX pathway suggest that PG does not contribute to cutaneous Vasodilation during WMTS.

Prostanoids contribute to cutaneous active vasodilation in humans.

The data suggest that prostanoids contribute to active vasodilation, but do not play a role during local thermal hyperemia.
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