Cutaneous blood flow responses in the forearms of Raynaud's patients induced by local cooling and intradermal injections of CGRP and histamine.

Brain, Susan D.; Petty, RG; Lewis, J. S.; Td, Williams

doi:10.1111/j.1365-2125.1990.tb05451.x

Cited by 26 publications

(15 citation statements)

References 17 publications

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“…These results suggest that it is an axon-reflex flare, observed by Lewis as a component of the triple response of the skin to injury (Lewis, 1927). Further, the flare response to endothelin is partially inhibited by the Hl-receptor antagonists chlorpheniramine (1 pug intradermally) and terfenadine (120 mg orally) (Crossman et al, 1991 (Brain et al, 1990;Crossman et al, 1991). Briefly the laser probe measured blood flow recorded as flux (number of red blood cells moving in the path of the laser beam multiplied by mean cell velocity) in a 1-2 mm2 area, for each reading.…”

Section: Introduction Methodsmentioning

confidence: 73%

Endothelin‐1 induces a histamine‐dependent flare in vivo, but does not activate human skin mast cells in vitro.

Brain¹,

Thomas²,

Crossman³

et al. 1992

Brit J Clinical Pharma

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The role of the mast cell in endothelin-1 induced flare has been investigated by in vivo and in vitro experiments. The intradermal injection of endothelin-1 (10 pmol) into human skin induced a pallor with surrounding axon-reflex flare which is similar to the flare response to histamine (1 nmol). At these doses, chosen to give identical flare areas, blood flow was increased in the area of the endothelin-induced flare over a longer period.A systemic Hl-receptor antagonist significantly inhibited the area of both flares, although blood flow in the remaining portion of the endothelin-induced flare remained raised.Endothelin-1 at concentrations up to 3 x 10-5 M failed to release histamine from human dispersed skin mast cells. We suggest from these results that a major component of endothelin-1 induced flare results from mast cell activation that is secondary to direct stimulation of sensory nerves by the peptide.

show abstract

Section: Introduction Methodsmentioning

confidence: 73%

Endothelin‐1 induces a histamine‐dependent flare in vivo, but does not activate human skin mast cells in vitro.

Brain¹,

Thomas²,

Crossman³

et al. 1992

Brit J Clinical Pharma

Self Cite

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“…Intravenous infusion of CGRP reverses the compromised digital cutaneous vascular insufficiency, as measured by laser Doppler flowmetry, and promoted healing of ulcers in four of five patients with severe Reynaud's syndrome secondary to connective tissue disease (257,556). Brain and colleagues (559) reported that these patients do not exhibit a diminished response to CGRP in the cutaneous microvasculature (496). The role of CGRP and agonists also needs to be explored in situations with other acute and chronic peripheral vascular occlusions.…”

Section: Peripheral Vascular Disease and Reynaud's Syndromementioning

confidence: 99%

Calcitonin gene-related peptide and its receptors: molecular genetics, physiology, pathophysiology, and therapeutic potentials

Wimalawansa¹

1996

Endocrine Reviews

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“…It is well established that the inducible isoform COX-2 is responsible for the biosynthesis of PGE 2 by activated monocytes/macrophages (2,3). PGE 2 is a potent vasodilator (4,5) that also prevents overactivation of cellular immunity (6 -8). It was also reported that PGE 2 exerts antiviral activities.…”

mentioning

confidence: 99%

EBV Suppresses Prostaglandin E2 Biosynthesis in Human Monocytes

Savard

Bélanger

Tremblay

et al. 2000

The Journal of Immunology

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It is well known that EBV has developed strategies to evade immune surveillance. Previously, EBV was shown to bind specifically to monocytes and regulate expression of proinflammatory mediators such as IL-1, IL-6, TNF-α, and leukotrienes. EBV was also found to affect phagocytosis of monocytes. In this study, we show that in addition to these effects, EBV suppresses the biosynthesis of PGE2, a pleiotropic immunomodulatory molecule that is synthesized by the dioxygenation of arachidonic acid via the cyclooxygenase (COX) pathway. This down-regulation of PGE2 formation involved the inhibition of the inducible COX-2 isoform expression both at the transcriptional and translational levels, whereas expression of the constitutive COX-1 isoform was unaltered. Furthermore, exposure of monocytes to EBV was found to impact on the NF-κB activation pathway, which plays an essential role in the induction of COX-2 in monocytes. The inhibition of PGE2 biosynthesis was relieved when the experiments were conducted in presence of phosphonoacetic acid, an inhibitor of herpesviruses DNA polymerase, indicating that viral replication and/or neosynthesized viral proteins were involved in this process. Thus, inhibition of PGE2 biosynthesis in monocytes may represent an additional mechanism underlying EBV pathogenicity.

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Cutaneous blood flow responses in the forearms of Raynaud's patients induced by local cooling and intradermal injections of CGRP and histamine.

Cited by 26 publications

References 17 publications

Endothelin‐1 induces a histamine‐dependent flare in vivo, but does not activate human skin mast cells in vitro.

Endothelin‐1 induces a histamine‐dependent flare in vivo, but does not activate human skin mast cells in vitro.

Calcitonin gene-related peptide and its receptors: molecular genetics, physiology, pathophysiology, and therapeutic potentials

EBV Suppresses Prostaglandin E2 Biosynthesis in Human Monocytes

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