scholarly journals ADP Receptor P2Y 12 Is Expressed in Vascular Smooth Muscle Cells and Stimulates Contraction in Human Blood Vessels

2004 ◽  
Vol 24 (10) ◽  
pp. 1810-1815 ◽  
Author(s):  
Anna-Karin Wihlborg ◽  
Lingwei Wang ◽  
Oscar Östberg Braun ◽  
Atli Eyjolfsson ◽  
Ronny Gustafsson ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Blood Vessels ◽  
Vascular Smooth Muscle Cells ◽  
Human Blood ◽  
Muscle Cells ◽  
Adp Receptor

Hydrogen peroxide mediates a transient vasorelaxation with tempol during oxidative stress

2007 ◽  
Vol 293 (4) ◽  
pp. H2085-H2092 ◽  
Author(s):  
Yifan Chen ◽  
Adam Pearlman ◽  
Zaiming Luo ◽  
Christopher S. Wilcox
Keyword(s):  
Oxidative Stress ◽  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Blood Vessels ◽  
Vascular Smooth Muscle Cells ◽  
Prolonged Exposure ◽  
Muscle Cells ◽  
Mesenteric Arteries

Tempol catalyzes the formation of H2O2 from superoxide and relaxes blood vessels. We tested the hypothesis that the generation of H2O2 by tempol in vascular smooth muscle cells during oxidative stress contributes to the vasorelaxation. Tempol and nitroblue tetrazolium (NBT) both metabolize superoxide in vascular smooth muscle cells, but only tempol generates H2O2. Rat pressurized mesenteric arteries were exposed for 20 min to the thromboxane-prostanoid receptor agonist, U-46619, or norepinephrine. During U-46619, tempol caused a transient dilation (22 ± 2%), whereas NBT was ineffective (2 ± 1%), and neither dilated vessels constricted with norepinephrine, which does not cause vascular oxidative stress. Neither endothelium removal nor blockade of K+ channels with 40 mM KCl affected the tempol-induced dilation, but catalase blunted the tempol dilation by 53 ± 7%. Tempol, but not NBT, increased H2O2 in rat mesenteric vessels detected with dichlorofluorescein. To test physiological relevance in vivo, topical application of tempol caused a transient dilation (184 ± 20%) of mouse cremaster arterioles exposed to angiotensin II for 30 min, which was not seen with NBT (9 ± 4%). The vasodilation to tempol was reduced by 68 ± 6% by catalase. We conclude that the transient relaxation of blood vessels by tempol after prolonged exposure to U-46619 or angiotensin II is mediated in part via production of H2O2 and is largely independent of the endothelium and potassium channels.

scholarly journals EPAC in Vascular Smooth Muscle Cells

2020 ◽  
Vol 21 (14) ◽  
pp. 5160 ◽  
Author(s):  
Nadine Wehbe ◽  
Suzanne Awni Nasser ◽  
Yusra Al-Dhaheri ◽  
Rabah Iratni ◽  
Alessandra Bitto ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Blood Vessels ◽  
Vascular Smooth Muscle Cells ◽  
Vascular Tone ◽  
Muscle Cells ◽  
Effector Proteins ◽  
Phenotypic Switching

Vascular smooth muscle cells (VSMCs) are major components of blood vessels. They regulate physiological functions, such as vascular tone and blood flow. Under pathological conditions, VSMCs undergo a remodeling process known as phenotypic switching. During this process, VSMCs lose their contractility and acquire a synthetic phenotype, where they over-proliferate and migrate from the tunica media to the tunica interna, contributing to the occlusion of blood vessels. Since their discovery as effector proteins of cyclic adenosine 3′,5′-monophosphate (cAMP), exchange proteins activated by cAMP (EPACs) have been shown to play vital roles in a plethora of pathways in different cell systems. While extensive research to identify the role of EPAC in the vasculature has been conducted, much remains to be explored to resolve the reported discordance in EPAC’s effects. In this paper, we review the role of EPAC in VSMCs, namely its regulation of the vascular tone and phenotypic switching, with the likely involvement of reactive oxygen species (ROS) in the interplay between EPAC and its targets/effectors.

Effect of calcitonin, hydrocortisone, and parathyroid hormone on canine bone blood vessels

1981 ◽  
Vol 241 (1) ◽  
pp. H91-H94 ◽  
Author(s):  
M. Driessens ◽  
P. M. Vanhoutte
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Blood Vessels ◽  
Vascular Smooth Muscle Cells ◽  
Perfusion Pressure ◽  
Muscle Cells ◽  
Ringer Solution ◽  
Dependent Inhibition ◽  
Dose Dependent

Experiments were designed to determine whether or not calcitonin, parathormone, and glucocorticoids have direct effects on the vascular smooth muscle cells of bone blood vessels. Tibias of mongrel dogs were isolated. The arteria nutriens was cannulated and perfused at constant flow with aerated Krebs-Ringer solution (37 degrees C). The perfusion pressure was continuously recorded. In unstimulated preparations calcitonin caused dose-dependent increases in perfusion pressure, indicating that it causes constriction of bone blood vessels. Parathormone did not affect basal perfusion; it did not significantly alter vasoconstrictions caused by the injection of norepinephrine indicating that the hormone has no direct effect on the vascular smooth muscle of bone blood vessels. Hydrocortisone, at low concentrations, augmented the constrictions caused by exogenous norepinephrine and periarterial nerve stimulation; at higher concentrations, hydrocortisone caused a dose-dependent inhibition of the response to adrenergic activation. The depressant effect of hydrocortisone was antagonized by propranolol, suggesting that the glucocorticoid facilitates beta-adrenergic relaxation of the vascular smooth muscle cells by catecholamines.

An extracellular source of heme can induce a significant heme oxygenase mediated relaxation in the rat aorta

2002 ◽  
Vol 80 (8) ◽  
pp. 761-765 ◽  
Author(s):  
S Hosein ◽  
G S Marks ◽  
J F Brien ◽  
B E McLaughlin ◽  
K Nakatsu
Keyword(s):  
Carbon Monoxide ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Blood Vessels ◽  
Vascular Smooth Muscle Cells ◽  
Heme Oxygenase ◽  
Muscle Cells ◽  
Rat Aorta ◽  
Bathing Medium

Carbon monoxide has been under active investigation for a role in controlling vascular tone throughout the last decade because of its ability to induce relaxation in blood vessels. The underlying mechanisms of this response are hypothesized to be mediated by soluble guanylyl cyclase (sGC) and, in some instances, KCa channels. The major source of CO in major blood vessels is the catabolic process of heme degradation, which is catalyzed by heme oxygenase (HO). This heme substrate could be derived from heme sources within vascular smooth muscle cells, such as heme proteins, or by uptake from the extracellular milieu. The current study shows that the isolated rat aorta relaxes upon exposure to pharmacological concentrations of heme in the bathing medium. This response was inhibited by an inhibitor of HO (tin protoporphyrin) and sGC (1-H-[1,2,4]-oxadiazolo[4,3-a]quinoxalin-1-one). These observations were interpreted to mean that vascular smooth muscle cells are capable of taking up and utilizing heme for the production of CO. Key words: carbon monoxide, heme oxygenase, heme, vascular smooth muscle.

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