Electrical coupling between smooth muscle cells and endothelial cells in pig coronary arteries

1996 ◽  
Vol 433 (3) ◽  
pp. 364 ◽  
Author(s):  
J.-L. Bény
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Coronary Arteries ◽  
Electrical Coupling ◽  
Muscle Cells ◽  
Pig Coronary Arteries

14,15-Dihydroxyeicosatrienoic acid relaxes bovine coronary arteries by activation of KCa channels

2002 ◽  
Vol 282 (5) ◽  
pp. H1656-H1664 ◽  
Author(s):  
William B. Campbell ◽  
Christine Deeter ◽  
Kathryn M. Gauthier ◽  
Richard H. Ingraham ◽  
J. R. Falck ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Coronary Arteries ◽  
Epoxide Hydrolase ◽  
Muscle Cells ◽  
Kca Channels ◽  
Vasodilator Activity ◽  
Inside Out ◽  
Isolated Smooth Muscle Cells

Epoxyeicosatrienoic acids (EETs) cause vascular relaxation by activating smooth muscle large conductance Ca2+-activated K+ (KCa) channels. EETs are metabolized to dihydroxyeicosatrienoic acids (DHETs) by epoxide hydrolase. We examined the contribution of 14,15-DHET to 14,15-EET-induced relaxations and characterized its mechanism of action. 14,15-DHET relaxed U-46619-precontracted bovine coronary artery rings but was approximately fivefold less potent than 14,15-EET. The relaxations were inhibited by charybdotoxin, iberiotoxin, and increasing extracellular K+ to 20 mM. In isolated smooth muscle cells, 14,15-DHET increased an iberiotoxin-sensitive, outward K+ current and increased KCa channel activity in cell-attached patches and inside-out patches only when GTP was present. 14,15-[14C]EET methyl ester (Me) was converted to 14,15-[14C]DHET-Me, 14,15-[14C]DHET, and 14,15-[14C]EET by coronary arterial rings and endothelial cells but not by smooth muscle cells. The metabolism to 14,15-DHET was inhibited by the epoxide hydrolase inhibitors 4-phenylchalcone oxide (4-PCO) and BIRD-0826. Neither inhibitor altered relaxations to acetylcholine, whereas relaxations to 14,15-EET-Me were increased slightly by BIRD-0826 but not by 4-PCO. 14,15-DHET relaxes coronary arteries through activation of KCa channels. Endothelial cells, but not smooth muscle cells, convert EETs to DHETs, and this conversion results in a loss of vasodilator activity.

scholarly journals EDHF: an update

2009 ◽  
Vol 117 (4) ◽  
pp. 139-155 ◽  
Author(s):  
Michel Félétou ◽  
Paul M. Vanhoutte
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Electrical Coupling ◽  
Muscle Cells ◽  
Therapeutic Interventions ◽  
K Channels ◽  
Acid Metabolites

The endothelium controls vascular tone not only by releasing NO and prostacyclin, but also by other pathways causing hyperpolarization of the underlying smooth muscle cells. This characteristic was at the origin of the term ‘endothelium-derived hyperpolarizing factor’ (EDHF). However, this acronym includes different mechanisms. Arachidonic acid metabolites derived from the cyclo-oxygenases, lipoxygenases and cytochrome P450 pathways, H2O2, CO, H2S and various peptides can be released by endothelial cells. These factors activate different families of K+ channels and hyperpolarization of the vascular smooth muscle cells contribute to the mechanisms leading to their relaxation. Additionally, another pathway associated with the hyperpolarization of both endothelial and vascular smooth muscle cells contributes also to endothelium-dependent relaxations (EDHF-mediated responses). These responses involve an increase in the intracellular Ca2+ concentration of the endothelial cells, followed by the opening of SKCa and IKCa channels (small and intermediate conductance Ca2+-activated K+ channels respectively). These channels have a distinct subcellular distribution: SKCa are widely distributed over the plasma membrane, whereas IKCa are preferentially expressed in the endothelial projections toward the smooth muscle cells. Following SKCa activation, smooth muscle hyperpolarization is preferentially evoked by electrical coupling through myoendothelial gap junctions, whereas, following IKCa activation, K+ efflux can activate smooth muscle Kir2.1 and/or Na+/K+-ATPase. EDHF-mediated responses are altered by aging and various pathologies. Therapeutic interventions can restore these responses, suggesting that the improvement in the EDHF pathway contributes to their beneficial effect. A better characterization of EDHF-mediated responses should allow the determination of whether or not new drugable targets can be identified for the treatment of cardiovascular diseases.

scholarly journals APOPTOSIS CELLS OF CORONARY ARTERY WALL AS DEVELOPING AND PROGRESSING FACTOR OF CORONARY SCLEROSIS

2013 ◽  
Vol 68 (9) ◽  
pp. 22-26
Author(s):  
T. E. Vladimirskaya ◽  
I. A. Shved ◽  
S. G. Krivorot
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Coronary Artery ◽  
Smooth Muscle Cells ◽  
Coronary Arteries ◽  
Muscle Cells ◽  
Artery Wall ◽  
Paraffin Sections ◽  
Early Stages ◽  
Coronary Artery Wall

Objective: to study apoptosis of individual cellular components of the vascular wall of coronary arteries at different morphological stages of atherosclerosis. Material and methods. The study was performed on coronary arteries taken from 52 deceased patients with atherosclerosis and coronary heart disease at different stages of atherogenesis. For morphological study prepared paraffin sections, which were stained for morphological studies were prepared paraffin sections, which were stained with hematoxylin and eosin, by Van Gieson, Masson, on lipids with Sudan black B, according to Van Cossu. .To determine apoptosis, TUNEL method used in paraffin sections. Apoptotic index (AI) was calculated by TUNEL-positive cells and the average inner shell coronary artery around the perimeter each with increasing microscopic 1000. Results. Investigation showed significant apoptosis (p 0.05) increase in AI smooth muscle, endothelial cells, macrophages in the coronary arteries affected by atherosclerosis compared to intact control group vascular segments significant reduction AI endothelial, smooth muscle cells and macrophages (p  0,05) traced from the early stages of atherogenic disorders to atheromatosis. Conclusions. It is established that apoptosis of smooth muscle cells, macrophages and endothelial cells is the most intensive on early stages of atherosclerotic process. In process of progressing of atherosclerosis intensity and prevalence of apoptosis of coronary artery wall cells decreases, and processes of necrosis becomes predominant. Apoptosis of coronary artery wall cells is valuable in increasing the zones of atheromatosis, plaque destabilizations, and also increases the risk of thrombosis and ulcerations. 

Role of smooth muscle cells on endothelial cell cytosolic free calcium in porcine coronary arteries

2001 ◽  
Vol 281 (3) ◽  
pp. H1156-H1162 ◽  
Author(s):  
Stéphane Budel ◽  
Alexander Schuster ◽  
Nikos Stergiopoulos ◽  
Jean-Jacques Meister ◽  
Jean-Louis Bény
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Coronary Arteries ◽  
Calcium Concentration ◽  
Muscle Cells ◽  
Free Calcium ◽  
Cytosolic Free Calcium ◽  
Free Calcium Concentration ◽  
Cytosolic Free Calcium Concentration

We tested the hypothesis that the cytosolic free calcium concentration in endothelial cells is under the influence of the smooth muscle cells in the coronary circulation. In the left descending branch of porcine coronary arteries, cytosolic free calcium concentration ([Ca2+]i) was estimated by determining the fluorescence ratio of two calcium probes, fluo 4 and fura red, in smooth muscle and endothelial cells using confocal microscopy. Acetylcholine and potassium, which act directly on smooth muscle cells to increase [Ca2+]i, were found to indirectly elevate [Ca2+]i in endothelial cells; in primary cultures of endothelial cells, neither stimulus affected [Ca2+]i, yet substance P increased the fluorescence ratio twofold. In response to acetylcholine and potassium, isometric tension developed by arterial strips with intact endothelium was attenuated by up to 22% ( P < 0.05) compared with strips without endothelium. These findings suggest that stimuli that increase smooth muscle [Ca2+]i can indirectly influence endothelial cell function in porcine coronary arteries. Such a pathway for negative feedback can moderate vasoconstriction and diminish the potential for vasospasm in the coronary circulation.

scholarly journals Pathogenesis of atherosclerosis in the tunica intima, media, and adventitia of coronary arteries: An updated review

2019 ◽  
Author(s):  
Aleksandra Milutinović ◽  
Dušan Šuput ◽  
Ruda Zorc-Pleskovič
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Coronary Arteries ◽  
Muscle Cells ◽  
Chronic Inflammatory Disease ◽  
Elastic Membrane ◽  
Atherosclerotic Plaques ◽  
Perivascular Adipose Tissue ◽  
Tunica Intima

Atherosclerosis is a chronic inflammatory disease of arteries and it affects the structure and function of all three layers of the coronary artery wall. Current theories suggest that the dysfunction of endothelial cells is one of the initial steps in the development of atherosclerosis. The view that the tunica intima normally consists of a single layer of endothelial cells attached to the subendothelial layer and internal elastic membrane has been questioned in recent years. The structure of intima changes with age and it becomes multilayered due to migration of smooth muscle cells from the media to intima. At this stage, the migration and proliferation of smooth muscle cells do not cause pathological changes in the intima. The multilayering of intima is classically considered to be an important stage in the development of atherosclerosis, but in fact atherosclerotic plaques develop only focally due to the interplay of various processes that involve the resident and invading inflammatory cells. The tunica media consists of multiple layers of smooth muscle cells that produce the extracellular matrix, and this layer normally does not contain microvessels. During the development of atherosclerosis, the microvessels from the tunica adventitia or from the lumen may penetrate thickened media to provide nutrition and oxygenation. According to some theories, the endothelial dysfunction of these nutritive vessels may significantly contribute to the atherosclerosis of coronary arteries. The adventitia contains fibroblasts, progenitor cells, immune cells, microvessels, and adrenergic nerves. The degree of inflammatory cell infiltration into the adventitia, which can lead to the formation of tertiary lymphoid organs, correlates with the severity of atherosclerotic plaques. Coronary arteries are surrounded by perivascular adipose tissue that also participates in the atherosclerotic process.

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