Attenuation of Histamine‐Induced Endothelial Permeability Responses after Pacing‐Induced Heart Failure: Role for Endogenous Catecholamines

Dyess, Donna L.; Hunter, Justin L.; LAKEY, JAMES R.; Moyer, Darlene; Dougherty, F. C.; Townsley, Mary I.

doi:10.1111/j.1549-8719.2000.tb00130.x

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Skin's Beta2 Adrenergic Receptors (β-Ars)1

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Cited by 9 publications

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“…The β-adrenergic (β-ARs) agonists are capable of modulating the two distinct components of keratinocyte directional migration via divergent signaling pathways: 1) migration rate via a cAMP-independent, mitogenactivated-protein-kinase-dependent pathway [57] and 2) galvanotaxis by a cAMP-dependent one. Previous data have shown that both endogenous and exogenous catecholamines act to attenuate the permeability response to various inflammatory mediators via β1- [58] and β2adrenoceptors [59] [60] [61] [62]. Additionally, because β-adrenergic agonists and antagonists modulate both keratinocyte migration and galvanotaxis, they could be valuable tools for controlling reepithelialization and restoration of barrier function, an essential component of the wound healing process.…”

Section: Skin's Beta2 Adrenergic Receptors (β-Ars)mentioning

confidence: 99%