Vasoactive peptides in the skin

Wallengren, Joanna

doi:10.1016/s0926-9959(98)94829-2

Cited by 69 publications

(96 citation statements)

References 34 publications

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“…As both CGRP and substance P are colocalized in nerve terminals in human skin (Wallengren, 1997), it is believed that upon stimulation they are released to increase vascular permeability and dilate adjacent blood vessels (Drummond, 2009). Likewise, these qualities seem to mimic the vasculature responses reported by Drummond (2009Drummond ( , 2010a, where the resultant vasodilatation of cutaneous blood vessels or nearby 'flare' (5-10 mm from stimulation site) ultimately provides an opportunity to disperse harmful threats that may disrupt healthy functioning.…”

Section: Sensory Nervesmentioning

confidence: 99%

“…Both groups observed an abolition of the biphasic increase in skin blood flow (SkBF), which ultimately rendered the vasodilator response insensitive to NOS inhibition. Sensory-nervemediated effects are thought to be produced via calcitonin gene-related peptide (CGRP) and substance P, and since both are colocalized in nerve terminals in human skin (Wallengren, 1997), it is believed that upon stimulation they are released to increase vascular permeability and dilate adjacent blood vessels (Drummond, 2009). Thus, a painful stimulus might invoke a sensory-nerve-mediated vasodilator response in an attempt to reduce thermal damage to the vasculature.…”

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confidence: 99%

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Sensory and sympathetic nerve contributions to the cutaneous vasodilator response from a noxious heat stimulus

Carter

Hodges

2011

Experimental Physiology

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We investigated the roles of sensory and noradrenergic sympathetic nerves on the cutaneous vasodilator response to a localized noxious heating stimulus. In two separate studies, four forearm skin sites were instrumented with microdialysis fibres, local heaters and laser-Doppler probes. Skin sites were locally heated from 33 to 42• C or rapidly to 44 • C (noxious). In the first study, we tested sensory nerve involvement using EMLA cream. Treatments were as follows: (1) control 42• C; (2) EMLA 42 • C; (3) control 44 • C; and (4) EMLA 44• C. At the EMLA-treated sites, the axon reflex was reduced compared with the control sites during heating to 42• C (P < 0.05). There were no differences during the plateau phase (P > 0.05). At both the sites heated to 44• C, the initial peak and nadir became indistinguishable, and the EMLA-treated sites were lower compared with the control sites during the plateau phase (P < 0.05). In the second study, we tested the involvement of noradrenergic sympathetic nerves in response to the noxious heating using bretylium tosylate (BT). Treatments were as follows: (1) • C sites, there was no apparent initial peak or nadir, but the plateau phase was reduced at the BT-treated sites (P < 0.05). These data suggest that both sympathetic nerves and sensory nerves are involved during the vasodilator response to a noxious heat stimulus.

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Section: Sensory Nervesmentioning

confidence: 99%

mentioning

confidence: 99%

Sensory and sympathetic nerve contributions to the cutaneous vasodilator response from a noxious heat stimulus

Carter

Hodges

2011

Experimental Physiology

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“…SP release may induce the co-release of CGRP, which in turn may enhance the action of SP, although CGRP may have longlasting effects. Moreover, the release of SP or CGRP may induce an increase in the levels of SP receptors (NK-1R) [32,41,42].…”

mentioning

confidence: 99%

The action of CGRP and SP on cultured skin fibroblasts

Hochman

Tucci-Viegas²,

Monteiro

et al. 2014

Open Life Sciences

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“…Neurokinin A is a tachykinin with broad tissue distribution and function (26,33,36). In skin and immune cells, neurokinin A exerts a physiological role in modulating cell proliferation, cytokine production, antigen presentation, and inflammation of the epidermal and dermal layers (32).…”

Section: Resultsmentioning

confidence: 99%

Specificity of a Vibrio vulnificus Aminopeptidase toward Kinins and Other Peptidyl Substrates

Richards

Núñez

2006

J Bacteriol

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Recently, phosphoglucose isomerase with a lysyl aminopeptidase (PGI-LysAP) activity was identified in Vibrio vulnificus. In this paper, we demonstrate the proteolytic cleavage of human-derived peptides by PGILysAP of V. vulnificus using three approaches: (i) a quantitative fluorescent ninhydrin assay for free lysine, (ii) matrix-assisted laser desorption ionization-two-stage time of flight mass spectrometry (MALDI-TOF-TOF), and (iii) Tricine gel electrophoresis. PGI-LysAP hydrolyzed bradykinin, Lys-bradykinin, Lys-(des-Arg 9 )-bradykinin, neurokinin A, Met-Lys-bradykinin, histatin 8, and a myosin light chain fragment. We detected the proteolytic release of free L-lysine from peptide digests using a rapid, simple, sensitive, and quantitative fluorescent ninhydrin assay, and results were confirmed by MALDI-TOF-TOF. The use of the fluorescent ninhydrin assay to quantitatively detect free lysine hydrolyzed from peptides is the first application of its kind and serves as a paradigm for future studies. The visualization of peptide hydrolysis was accomplished by Tricine gel electrophoresis. Proteolytic processing of kinins alters their affinities toward specific cellular receptors and initiates signal transduction mechanisms responsible for inflammation, vasodilation, and enhanced vascular permeability. By applying novel approaches to determine the proteolytic potential of bacterial enzymes, we demonstrate that PGI-LysAP has broad exopeptidase activity which may enhance V. vulnificus invasiveness by altering peptides involved in signal transduction pathways.Vibrio vulnificus is a naturally occurring marine bacterium indigenous to temperate and tropical estuarine environments. It has two routes of transmission: wound infections and the ingestion of contaminated seafood, especially raw oysters. During summer months, nearly 100% of the oysters harvested from the Gulf of Mexico contain V. vulnificus (9). Liver cirrhosis, hemochromatosis, diabetes, kidney disease, and immune disorders predispose individuals to V. vulnificus infection via the food-borne route (4, 24); however, even seemingly healthy individuals are susceptible to V. vulnificus through wound infections (24). Symptoms include fever, chills, hypotension, and the development of secondary bullous skin lesions. Septicemia is common, and death can occur within 24 h after contact with the pathogen (8, 24). Mortality rates for V. vulnificus infections are approximately 60% in the United States (15) but are somewhat higher in Asian countries (14,25).Over the past two decades, numerous virulence factors have been identified in V. vulnificus based on cell culture and animal models; however, the validity of these models in assessing virulence has come into question (7). A case in point involves V. vulnificus protease, a well-characterized metalloprotease (23). In the mouse model, injection of this protease causes skin necrosis; however, knockout of the gene in V. vulnificus does not attenuate the symptoms in Vibrio-infected laboratory animals (34).Recently, we isolated a...

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Vasoactive peptides in the skin

Cited by 69 publications

References 34 publications

Sensory and sympathetic nerve contributions to the cutaneous vasodilator response from a noxious heat stimulus

Sensory and sympathetic nerve contributions to the cutaneous vasodilator response from a noxious heat stimulus

The action of CGRP and SP on cultured skin fibroblasts

Specificity of a Vibrio vulnificus Aminopeptidase toward Kinins and Other Peptidyl Substrates

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