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

  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},
  volume={98 2},
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… 

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Nitric Oxide and Prostaglandin Inhibition During Acetylcholine‐Mediated Cutaneous Vasodilation in Humans

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.



Role of nitric oxide in the vascular effects of local warming of the skin in humans.

The mechanism of cutaneous vasodilation by local warming requires NOS generation of NO, and effects of NO synthase (NOS) inhibition with NG-nitro-L-arginine methyl ester (L-NAME) on Vasodilation induced byLocal warming of skin in six subjects were examined.

Cutaneous active vasodilation in humans is mediated by cholinergic nerve cotransmission.

It is concluded that cholinergic nerve activation mediates cutaneous active vasodilation through release of an unknown cotransmitter, not through ACh.

Effects of nitric oxide synthase inhibition on cutaneous vasodilation during body heating in humans.

It is demonstrated that NO contributes modestly, but not consistently, to cutaneous vasodilation during body heating in humans, and this indicates that NO is not the only factor responsible for the dilation.

Nitric oxide and cutaneous active vasodilation during heat stress in humans.

Cutaneous active vasodilation requires functional NO synthase to achieve full expression as achieved by perfusion with the NO donor nitroprusside through the microdialysis probes, and L-NAME had no effect on sweat rate.

Role of nitric oxide in the regulation of microvascular perfusion in human skin in vivo

  • G. Clough
  • Medicine, Biology
    The Journal of physiology
  • 1999
The results demonstrate, by the use of microdialysis, that vasoactive mediators can be measured in healthy human skin in vivo and provide direct evidence that endogenous concentration of NO increases during the inflammatory weal and flare response to histamine and that the increase in dermal NO concentration is associated with increases in cGMP concentration and dermal vascular perfusion, thus confirming a role for NO in vasoregulation in human skin.

Is nitric oxide involved in cutaneous vasodilation during body heating in humans?

The neurotransmitter responsible for neurogenic vasodilation in human skin during body heating is unknown and whether the vasodilating substance nitric oxide (NO) is involved in this phenomenon is investigated.

Vascular and neural mechanisms of ACh-mediated vasodilation in the forearm cutaneous microcirculation.

The findings suggest that prostanoids do not contribute significantly to basal CuBF or endothelium-dependent vasodilation in the forearm microcirculation and, in contrast, prostanoid are mediators of the ACh-provoked axon reflex.

Studies with iontophoretic administration of drugs to human dermal vessels in vivo: cholinergic vasodilatation is mediated by dilator prostanoids rather than nitric oxide.

Dermal vasodilatation in response to iontophoresis of ACh is mediated predominately by a dilator prostanoid rather than by nitric oxide generation, which could complement existing invasive tests of endothelial function in future clinical studies.

Effects of atropine and L-NAME on cutaneous blood flow during body heating in humans.

The results indicate that neither sweating nor NO release via muscarinic receptor activation is essential to sustain cutaneous dilation during heating in humans.

Bradykinin does not mediate cutaneous active vasodilation during heat stress in humans.

It is concluded that bradykinin does not mediate cutaneous active vasodilation during hyperthermia, and HOE-140 did not alter SkBF responses to heat stress.