scholarly journals Cellular and ionic signal transduction mechanisms for the mechanical activation of renal arterial vascular smooth muscle.

1993 ◽  
Vol 4 (4) ◽  
pp. 986-996
Author(s):  
R J Roman ◽  
D R Harder
Keyword(s):  
Arachidonic Acid ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Vascular Smooth Muscle Cells ◽  
Vascular Tone ◽  
Calcium Concentration ◽  
Renal Arteries ◽  
Myogenic Response ◽  
Renal Vascular ◽  
Cytochrome P 450

Elevations in transmural pressure increase active vascular tone in arteries from most vascular beds, and this myogenic response has been shown to play an important role in the regulation of blood flow in the kidney and other organs. The myogenic response in isolated perfused arteries is associated with depolarization of vascular smooth muscle cells and a rise in intracellular calcium concentration, which is dependent on calcium influx through voltage-sensitive calcium channels. Recent studies have indicated that the myogenic response in renal arteries is associated with the activation of phospholipase C and that arachidonic acid potentiates, whereas inhibitors of cytochrome P-450 and protein kinase C attenuate, this response. Renal arteries produce 20-hydroxyeicosatetraenoic acid (20-HETE) via the cytochrome P-450 pathway when incubated with arachidonic acid. 20-HETE is a potent constrictor of canine and rat renal arterioles. It inhibits K+ channel activity, depolarizes renal vascular smooth muscle cells, and produces a sustained increase in intracellular calcium concentration. In this regard, the vasoconstrictor response to 20-HETE mimics the myogenic activation of renal arteries after elevations in transmural pressure. These studies suggest that the activation of phospholipase C and subsequent increases in the intracellular levels of diacylglycerol, 1,4,5 inositol triphosphate, and cytochrome P-450 metabolites of arachidonic acid may participate in the myogenic response of renal arteries and in the regulation of renal vascular tone.

scholarly journals Remanent cell traction force in renal vascular smooth muscle cells induced by integrin-mediated mechanotransduction

2013 ◽  
Vol 304 (4) ◽  
pp. C382-C391 ◽  
Author(s):  
Lavanya Balasubramanian ◽  
Chun-Min Lo ◽  
James S. K. Sham ◽  
Kay-Pong Yip
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Resistance ◽  
Vascular Smooth Muscle Cells ◽  
Traction Force ◽  
Muscle Cells ◽  
Myogenic Response ◽  
Cell Traction ◽  
Renal Vascular

It was previously demonstrated in isolated renal vascular smooth muscle cells (VSMCs) that integrin-mediated mechanotransduction triggers intracellular Ca2+ mobilization, which is the hallmark of myogenic response in VSMCs. To test directly whether integrin-mediated mechanotransduction results in the myogenic response-like behavior in renal VSMCs, cell traction force microscopy was used to monitor cell traction force when the cells were pulled with fibronectin-coated or low density lipoprotein (LDL)-coated paramagnetic beads. LDL-coated beads were used as a control for nonintegrin-mediated mechanotransduction. Pulling with LDL-coated beads increased the cell traction force by 61 ± 12% (9 cells), which returned to the prepull level after the pulling process was terminated. Pulling with noncoated beads had a minimal increase in the cell traction force (12 ± 9%, 8 cells). Pulling with fibronectin-coated beads increased the cell traction force by 56 ± 20% (7 cells). However, the cell traction force was still elevated by 23 ± 14% after the pulling process was terminated. This behavior is analogous to the changes of vascular resistance in pressure-induced myogenic response, in which vascular resistance remains elevated after myogenic constriction. Fibronectin is a native ligand for α5β1-integrins in VSMCs. Similar remanent cell traction force was found when cells were pulled with beads coated with β1-integrin antibody (Ha2/5). Activation of β1-integrin with soluble antibody also triggered variations of cell traction force and Ca2+ mobilization, which were abolished by the Src inhibitor. In conclusion, mechanical force transduced by α5β1-integrins triggered a myogenic response-like behavior in isolated renal VSMCs.

scholarly journals Ligation of α 5 β 1 ‐ integrins triggers Ca 2+ sparks in renal vascular smooth muscle cells

2006 ◽  
Vol 20 (4) ◽  
Author(s):  
Lavanya Balasubramanian ◽  
C.‐M. Lo ◽  
C.S. Landon ◽  
J.S.K. Sham ◽  
K.‐P. Yip
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Renal Vascular

EGF and TGF-beta regulate neutral endopeptidase expression in renal vascular smooth muscle cells

1997 ◽  
Vol 272 (6) ◽  
pp. C1836-C1843 ◽  
Author(s):  
P. L. Tharaux ◽  
A. Stefanski ◽  
S. Ledoux ◽  
J. M. Soleilhac ◽  
R. Ardaillou ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Growth Factor ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Transforming Growth Factor ◽  
Muscle Cells ◽  
Neutral Endopeptidase ◽  
Tgf Beta ◽  
Renal Vascular

We recently reported that neutral endopeptidase (NEP) expression on renal vascular smooth muscle cells (VSMC) was downregulated in the presence of serum. Here we examine the role of epidermal growth factor (EGF) and transforming growth factor-beta 1 (TGF-beta) in this downregulation and the consequences of the changes in NEP activity on their mitogenic effects. EGF inhibited NEP activity, whereas TGF-beta was stimulatory. Expression of the enzyme was studied by measuring the binding of [125I]RB-104, a specific NEP inhibitor, and the fluorescence intensity of NEP-labeled cells. Both parameters were decreased by EGF and were increased by TGF-beta. NEP mRNA expression in EGF-treated cells was reduced after 48 h. In contrast, it was increased in TGF-beta-treated cells. Interestingly, NEP inhibition influenced the mitogenic effect of EGF. Indeed, thiorphan, an NEP inhibitor, and an anti-NEP antibody decreased EGF-dependent [3H]thymidine incorporation and cell proliferation by approximately 50%. TGF-beta had no effect on VSMC growth. These results indicate that EGF but not TGF-beta participates in the downregulatory potency of serum on NEP expression in VSMC. They also demonstrate that the full effect of EGF on VSMC proliferation depends on intact NEP activity.

Secretion of Brain Natriuretic Peptide in Cultured Human Coronary Vascular Smooth Muscle Cells

2000 ◽  
Vol 6 (S2) ◽  
pp. 598-599
Author(s):  
J. Lin ◽  
C. Wei
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Brain Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Vascular Smooth Muscle Cells ◽  
Vascular Tone ◽  
Culture Media ◽  
Muscle Cells ◽  
Ventricular Myocardium

Brain natriuretic peptide (BNP) is a peptide of cardiac origin which regulates plasma volume as well as vascular tone and growth. Recently, we have reported that brain natriuretic peptide is a potent inhibitor of endothelin-1-mediated proliferation in human coronary vascular smooth muscle cells (HCoVSMC). While brain natriuretic peptide has been reported to be produced and released from atrial and ventricular myocardium, we hypothesize that brain natriuretic peptide may be present and secreted from human coronary vascular smooth muscle cells.Therefore, the present study was designed to investigate the secretion of brain natriuretic peptide in cultured human coronary vascular smooth muscle cells (HCoVSMC: Clonetics, San Diego, CA). The concentration of brain natriuretic peptide, and its second messenger cGMP, in culture media (48 hours) was determined by radioimmunoassay (Phoenix, Mountain View, CA). The presence of brain natriuretic peptide was determined by immunohistochemical staining using a human brain natriuretic peptide polyclonal antibody.

Codonopsis lanceolata Contributes to Ca2+ Homeostasis by Mediating SOCE and PLC/IP3 Pathways in Vascular Endothelial and Smooth Muscle Cells

Planta Medica ◽  
2020 ◽  
Vol 86 (18) ◽  
pp. 1345-1352
Author(s):  
Min Kyung Kim ◽  
A Young Han ◽  
You Kyoung Shin ◽  
Kwang-Won Lee ◽  
Geun Hee Seol
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Calcium Concentration ◽  
Muscle Cells ◽  
Cytosolic Calcium ◽  
Cytosolic Calcium Concentration ◽  
Lancemaside A

Abstract Codonopsis lanceolata has been widely used as an anti-inflammatory and anti-lipogenic agent in traditional medicine. Recently, C. lanceolata was reported to prevent hypertension by improving vascular function. This study evaluated the effects of C. lanceolata and its major component lancemaside A on cytosolic calcium concentration in vascular endothelial cells and vascular smooth muscle cells. Cytosolic calcium concentration was measured using fura-2 AM fluorescence. C. lanceolata or lancemaside A increased the cytosolic calcium concentration by releasing Ca2+ from the endoplasmic reticulum and sarcoplasmic reticulum and by Ca2+ entry into endothelial cells and vascular smooth muscle cells from extracellular sources. The C. lanceolata- and lancemaside A-induced cytosolic calcium concentration increases were significantly inhibited by lanthanum, an inhibitor of non-selective cation channels, in both endothelial cells and vascular smooth muscle cells. Moreover, C. lanceolata and lancemaside A significantly inhibited store-operated Ca2+ entry under pathological extracellular Ca2+ levels. In Ca2+-free extracellular fluid, increases in the cytosolic calcium concentration induced by C. lanceolata or lancemaside A were significantly inhibited by U73122, an inhibitor of phospholipase C, and 2-APB, an inositol 1,4,5-trisphosphate receptor antagonist. In addition, dantrolene treatment, which inhibits Ca2+ release through ryanodine receptor channels, also inhibited C. lanceolata- or lancemaside A-induced increases in the cytosolic calcium concentration through the phospholipase C/inositol 1,4,5-trisphosphate pathway. These results suggest that C. lanceolata and lancemaside A increase the cytosolic calcium concentration through the non-selective cation channels and phospholipase C/inositol 1,4,5-trisphosphate pathways under physiological conditions and inhibit store-operated Ca2+ entry under pathological conditions in endothelial cells and vascular smooth muscle cells. C. lanceolata or lancemaside A can protect endothelial cells and vascular smooth muscle cells by maintaining cytosolic calcium concentration homeostasis, suggesting possible applications for these materials in diets for preventing vascular damage.

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