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Vasoactive Peptides (vasoactive + peptide)
Selected AbstractsThe Neurogenic Vasodilator Response to Endothelin-1: A Study in Human Skin In VivoEXPERIMENTAL PHYSIOLOGY, Issue 6 2000Ruwani Katugampola We have investigated the mediators and mechanisms underlying the vasodilator effects of the potent vasoactive peptide, endothelin-1 (ET-1) and its isomers ET-2 and ET-3 in human skin, in vivo, using cutaneous microdialysis to quantify the release of mediators within the dermal response and scanning laser Doppler imaging to measure changes in blood flux. The effects of local anaesthesia, inhibition of nitric oxide synthase (NOS) by L-NAME and ET receptor blockade on the ET-induced vascular response were also investigated. ET-1, -2 and -3 all caused a dose-dependent area of pallor surrounded by a long-lasting flare which was accompanied by a short-lived burning pruritus. The concentration of nitric oxide (NO) in dialysate collected within the pallor response to 5 ,M ET-1 (1.43 ± 0.64 ,M, n = 5) was not significantly different from baseline levels collected prior to injection (0.86 ± 0.38 ,M) whilst that in the flare increased to reach a peak value of 2.28 ± 0.61 ,M at between 4 and 10 min after intradermal injection (P < 0.004). Pretreatment with local anaesthetic slowed the development of the flare and significantly reduced its size by up to 52% at 20 min after injection (P < 0.05) but had no significant effect on the central pallor. L-NAME, delivered by dialysis also caused a significant reduction in the ET-1-induced flare (P < 0.005). Bosentan, the non-selective ETA/ETB antagonist, when given by dialysis at the site of injection, reduced the area of both the ET-1-induced pallor and surrounding flare by 41 and 26%, respectively. No significant increase in tissue histamine was measured within either the pallor or flare response to ET-1, -2 or -3. Together these data confirm that the vasodilator response to endothelin-1 in human skin is neurogenic in origin and that it is in part mediated by the local release of nitric oxide. There appears to be little evidence for the involvement of mast cell-derived histamine in the initiation or modulation of ET-induced vasodilatation, in vivo. [source] Diet-induced obesity in Sprague,Dawley rats causes microvascular and neural dysfunctionDIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue 4 2010Eric P. Davidson Abstract Background The objective of this study was to determine the effect of diet-induced obesity (DIO) on microvascular and neural function. Methods Rats were fed a standard or high fat diet for up to 32 weeks. The following measurements were carried out: vasodilation in epineurial arterioles using videomicroscopy, endoneurial blood flow using hydrogen clearance, nerve conduction velocity using electrical stimulation, size,frequency distribution of myelinated fibres of the sciatic nerve, intraepidermal nerve fibre density using confocal microscopy and thermal nociception using the Hargreaves method. Results Rats fed a high fat diet for 32 weeks developed sensory neuropathy, as indicated by slowing of sensory nerve conduction velocity and thermal hypoalgesia. Motor nerve conduction velocity and endoneurial blood flow were not impaired. Mean axonal diameter of myelinated fibres of the sciatic nerve was unchanged in high fat-fed rats compared with that in control. Intraepidermal nerve fibre density was significantly reduced in high fat-fed rats. Vascular relaxation to acetylcholine and calcitonin gene-related peptide was decreased and expression of neutral endopeptidase (NEP) increased in epineurial arterioles of rats fed a high fat diet. In contrast, insulin-mediated vascular relaxation was increased in epineurial arterioles. NEP activity was significantly increased in the skin of the hindpaw. Markers of oxidative stress were increased in the aorta and serum of high fat-fed rats but not in epineurial arterioles. Conclusion Chronic obesity causes microvascular and neural dysfunction. This is associated with increased expression of NEP but not oxidative stress in epineurial arterioles. NEP degrades vasoactive peptides, which may explain the decrease in microvascular function. Copyright © 2010 John Wiley & Sons, Ltd. [source] Hypoxia is an inducer of vasodilator agents in peritoneal macrophages of cirrhotic patientsHEPATOLOGY, Issue 5 2002Pilar Cejudo-Martín The aim of the investigation was to assess whether hypoxia induces the production of endogenous vasoactive peptides in macrophages of cirrhotic patients with ascites because low tissue oxygenation is a relatively frequent event in these patients. Peritoneal macrophages were isolated from ascites, seeded on well plates, and cultured at different times under hypoxic (5% O2) or normoxic conditions (21% O2). Then, accumulation of vasoactive peptides sensitive to hypoxia including endothelin-1 (ET-1), vascular endothelial growth factor (VEGF), and adrenomedullin (ADM) was measured. Only VEGF and ADM were constitutively secreted, and hypoxia further stimulated the release of these vasodilator peptides. In concordance, increased messenger RNA (mRNA) levels of VEGF and ADM were found at culturing macrophages in hypoxia. This characteristic response was not observed in circulating monocytes of either cirrhotic patients or healthy subjects. Next the expression of the transcription factor, hypoxia inducible factor 1 (HIF-1), was analyzed. Expression of HIF-1, and HIF-1, messengers and HIF-1, protein subunit remained unchanged regardless of O2 tension, whereas HIF-1, protein subunit was overexpressed under hypoxic conditions. Moreover, conditioned medium from macrophages cultured under hypoxic conditions promoted a larger nitric oxide (NO) release in endothelial cells than that of normoxic macrophages. In conclusion, these data indicate that hypoxia induces the synthesis of VEGF and ADM in macrophages of cirrhotic patients, likely through HIF-1,enhanced transcriptional activity. These data suggest that a local reduction in O2 tension could enhance the synthesis of macrophage-derived vasodilators, thus aggravating the circulatory disturbance of these patients. [source] Anti-aging properties of resveratrol: review and report of a potent new antioxidant skin care formulationJOURNAL OF COSMETIC DERMATOLOGY, Issue 1 2008Richard A Baxter MD Summary Resveratrol, an antioxidant polyphenol from red wine, has been the subject of intense interest in recent years due to a range of unique anti-aging properties. These include cardiovascular benefits via increased nitric oxide production, down-regulation of vasoactive peptides, lowered levels of oxidized low-density lipoprotein, and cyclooxygenase inhibition; possible benefits on Alzheimer's disease by breakdown of beta-amyloid and direct effects on neural tissues; phytohormonal actions; anticancer properties via modulation of signal transduction, which translates into anti-initiation, antipromotion, and antiprogression effects; antimicrobial effects; and sirtuin activation, which is believed to be involved in the caloric restriction-longevity effect. Here we report a resveratrol-based skin care formulation, with 17 times greater antioxidant activity than idebenone. The role of resveratrol in prevention of photoaging is reviewed and compared with other antioxidants used in skin care products. [source] The human placenta from heavy smokers: evaluation of vasoactive peptides by immunohistochemistry,APMIS, Issue 1 2007H. V. CLAUSEN The study aimed to demonstrate the expression of nitric oxide converting enzyme, nitric oxide synthase (e-NOS), and endothelin-1 (Et-1) in formalin-fixed paraffin-embedded placental tissue, and to demonstrate a difference in staining intensity between heavy smokers and non-smokers. Term placentas from pregnancies from otherwise healthy women smoking 15 or more cigarettes per day (heavy smokers) and term placentas from a matching group of non-smokers were included. The antibodies for Et-1 and e-NOS are recommended for cryostat sections. We evaluated the antibodies on paraffin-embedded tissue combined with the streptavidin-biotin-peroxidase technique. Et-1 and e-NOS were demonstrated in the placental vasculature, the trophoblast, and the amnion. A blinded comparative study showed no reproducible significant differences in the staining intensity of the antigen-antibody reaction to Et-1 and e-NOS between the two groups. [source] | ||||||||||