A TRPC-like non-selective cation current activated by α1-adrenoceptors in rat mesenteric artery smooth muscle cells

Cell Calcium ◽  
2006 ◽  
Vol 40 (1) ◽  
pp. 29-40 ◽  
Author(s):  
Andrew J. Hill ◽  
Jane M. Hinton ◽  
Hongwei Cheng ◽  
Zhan Gao ◽  
David O. Bates ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Mesenteric Artery ◽  
Muscle Cells ◽  
Cation Current ◽  
Rat Mesenteric Artery

Large-conductance Ca2+-activated K+ currents blocked and impaired by homocysteine in human and rat mesenteric artery smooth muscle cells

Life Sciences ◽  
2007 ◽  
Vol 80 (22) ◽  
pp. 2060-2066 ◽  
Author(s):  
Benzhi Cai ◽  
Dongmei Gong ◽  
Zhenwei Pan ◽  
Yu Liu ◽  
Hong Qian ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Mesenteric Artery ◽  
Muscle Cells ◽  
Rat Mesenteric Artery ◽  
K Currents

The pro-oxidant role of methylglyoxal in mesenteric artery smooth muscle cells

2005 ◽  
Vol 83 (1) ◽  
pp. 63-68 ◽  
Author(s):  
Lingyun Wu
Keyword(s):  
Oxidative Stress ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Mesenteric Artery ◽  
Advanced Glycation Endproducts ◽  
Muscle Cells ◽  
Heme Oxygenase 1 ◽  
Rat Mesenteric Artery ◽  
Cultured Smooth Muscle Cells

Methylglyoxal (MG), a highly reactive metabolite of glucose, causes non-enzymatic glycation of proteins to form irreversible advanced glycation endproducts (AGEs). The present study investigated whether methylglyoxal induced oxidative stress and activated nuclear factor kappa B (NF-κB) in freshly isolated and cultured smooth muscle cells (SMCs) from rat mesenteric artery. The treatment of cells with MG (50 or 100 µmol/L) induced a significant increase in AGE formation and oxidation of DCF. MG-enhanced generation of AGEs and the oxidation of DCF was markedly inhibited by antioxidant n-acetylcysteine (NAC, 600 µmol/L). MG at a concentration of 100 µmol/L increased the heme-oxygenase-1 expression in these cells. Moreover, MG activated NF-κB p65, indicated by an increased im muno cytochemistry stain for NF-κB p65 located in the nucleus after the treatment of mesenteric artery SMCs with MG. MG-induced activation of NF-κB p65 was inhibited by NAC. In summary, MG significantly increases oxidative stress and activates NF-κB p65 in mesenteric artery SMCs. The pro-oxidant role of methylglyoxal may contribute to various pathological changes of SMCs from resistance arteries.Key words: methylglyoxal, oxidative stress, NF-κB p65, vascular smooth muscle cells, mesenteric artery.

Hydrogen sulfide-induced relaxation of resistance mesenteric artery beds of rats

2004 ◽  
Vol 287 (5) ◽  
pp. H2316-H2323 ◽  
Author(s):  
Youqin Cheng ◽  
Joseph Fomusi Ndisang ◽  
Guanghua Tang ◽  
Kun Cao ◽  
Rui Wang
Keyword(s):  
Smooth Muscle ◽  
Hydrogen Sulfide ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Mesenteric Artery ◽  
Muscle Cells ◽  
Mesenteric Arteries ◽  
Vascular Effects ◽  
Rat Mesenteric Artery

Hydrogen sulfide (H2S) has been shown recently to function as an important gasotransmitter. The present study investigated the vascular effects of H2S, both exogenously applied and endogenously generated, on resistance mesenteric arteries of rats and the underlying mechanisms. Both H2S and NaHS evoked concentration-dependent relaxation of in vitro perfused rat mesenteric artery beds (MAB). The sensitivity of MAB to H2S (EC50, 25.2 ± 3.6 μM) was about fivefold higher than that of rat aortic tissues. Removal of endothelium or coapplication of charybdotoxin and apamin to endothelium-intact MAB significantly reduced the vasorelaxation effects of H2S. The H2S-induced relaxation of MAB was partially mediated by ATP-sensitive K+ (KATP) channel activity in vascular smooth muscle cells. Pinacidil (EC50, 1.7 ± 0.1 μM, n = 6) mimicked, but glibenclamide (10 μM, n = 6) suppressed, the vasorelaxant effect of H2S. KATP channel currents in isolated mesenteric artery smooth muscle cells were significantly augmented by H2S. l-Cysteine, a substrate of cystathionine-γ-lyase (CSE), at 1 mM increased endogenous H2S production by sixfold in rat mesenteric artery tissues and decreased contractility of MAB. dl-Propargylglycine (a blocker of CSE) at 10 μM abolished l-cysteine-dependent increase in H2S production and relaxation of MAB. Our results demonstrated a tissue-specific relaxant response of resistance arteries to H2S. The stimulation of KATP channels in vascular smooth muscle cells and charybdotoxin/apamin-sensitive K+ channels in vascular endothelium by H2S represents important cellular mechanisms for H2S effect on MAB. Our study also demonstrated that endogenous CSE can generate sufficient H2S from exogenous l-cysteine to cause vasodilation. Future studies are merited to investigate direct contribution of endogenous H2S to regulation of vascular tone.

scholarly journals Extra Virgin Olive Oil Phenols Dilate the Rat Mesenteric Artery by Activation of BKCa2+ Channels in Smooth Muscle Cells

Molecules ◽  
2020 ◽  
Vol 25 (11) ◽  
pp. 2601
Author(s):  
Rossana D’Agostino ◽  
Laura Barberio ◽  
MariaCarmela Gatto ◽  
Innocenzo Muzzalupo ◽  
Maurizio Mandalà
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Olive Oil ◽  
Mesenteric Artery ◽  
Virgin Olive Oil ◽  
Muscle Cells ◽  
Extra Virgin Olive Oil ◽  
Bioactive Molecules ◽  
Hypotensive Activity ◽  
Rat Mesenteric Artery

Accumulating evidence has shown the beneficial health effects of extra virgin olive oil (EVOO) consumption in reducing blood pressure and preventing the risk of developing hypertension. Some studies associate the hypotensive activity of EVOO to a minor component—the phenols. This study was designed to investigate the effects of EVOO phenols on the rat resistance mesenteric artery (MA) and to find out the possible vascular pathways involved. The experiments were carried out using a pressurized myograph, which allowed the effects of phenols on isolated MA to be tested under different conditions: (a) with endothelium removed; (b) with inhibition of nitric oxide synthase by Nω-Nitro-l-arginine methyl ester hydrochloride (l-NAME, 10−4 M) + Nω-Nitro-l-arginine (l-NNA, 10−4 M); (c) with inhibition of cyclooxygenase by indomethacin (10−5 M); (d) with inhibition of guanylate cyclase by 1H-[1,2,4]Oxadiazolo[4,3-a]quinoxalin-1-one (ODQ,10−5 M) or adenylate cyclase by 9-(Tetrahydro-2′-furyl)adenine (SQ, 10−5 M); (e) with depolarization by high potassium chloride (40 mM); and (f) with inhibition of the large conductance Ca2+–potassium channels (BKCa2+) with paxilline (10−5 M). EVOO phenols induce vasodilation of the endothelium, mediated by a direct effect on smooth muscle cells (SMC) by activation of BKCa2+ channels, an action by which phenols can regulate the vascular tone of the resistance artery. Phenols can be regarded as bioactive molecules that may contribute to the antihypertensive effects of EVOO.

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