scholarly journals Mineralocorticoid Receptor in Calcium Handling of Vascular Smooth Muscle Cells

2018 ◽  
Author(s):  
Rogelio Salazar-Enciso ◽  
Nohemi A. Camacho-Concha ◽  
Thassio R. Mesquita ◽  
Débora Falcón ◽  
Jean-Pierre Benitah ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Mineralocorticoid Receptor ◽  
Muscle Cells ◽  
Calcium Handling

Enhanced proliferation and altered calcium handling in RGS2-deficient vascular smooth muscle cells

2014 ◽  
Vol 34 (6) ◽  
pp. 476-483 ◽  
Author(s):  
Abdul Momen ◽  
Talat Afroze ◽  
Al-Muktafi Sadi ◽  
Amir Khoshbin ◽  
Hangjun Zhang ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Calcium Handling

Delineating the receptor mechanisms underlying the rapid vascular contractile effects of aldosterone and estradiol

2011 ◽  
Vol 89 (9) ◽  
pp. 655-663 ◽  
Author(s):  
Robert Gros ◽  
Qingming Ding ◽  
Mark Davis ◽  
Rasha Shaikh ◽  
Bonan Liu ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Mineralocorticoid Receptor ◽  
Time Course ◽  
Cardiovascular Effects ◽  
Muscle Cells ◽  
Smooth Muscle Contraction ◽  
Cell Assays

It is increasingly appreciated that steroid hormones such as aldosterone and estradiol can mediate important cardiovascular effects. Many of these effects occur over a time course not consistent with the genomic actions of these hormones acting through classical nuclear receptors / transcription factors. Further, multiple receptors have been implicated in mediating these rapid effects of both aldosterone and estradiol, including a newly appreciated G-protein-coupled receptor, GPR30. In previous studies we demonstrated that both aldosterone and estradiol mediate contraction in vascular smooth muscle cells, as assessed in single cell assays. However, the receptor mechanisms underlying these effects remained unclear. Therefore, we studied the actions of estradiol and aldosterone on rat aortic vascular smooth muscle cells. Both aldosterone and estradiol mediated a concentration-dependent increase in contraction, as assessed in substrate deformation assays with EC50s in the range of nanomoles per litre. These effects paralleled increased myosin light chain phosphorylation. The effects of aldosterone were inhibited by the mineralocorticoid selective antagonist eplerenone. Further, aldosterone’s contractile effects were enhanced by increased expression of the mineralocorticoid receptor. The contractile effects of estradiol were inhibited by estrogen receptor (ER)-selective antagonists, tamoxifen, and ICI 182780, as well as eplerenone. Further, estradiol’s effects were enhanced by the increased expression of both ERα and the mineralocorticoid receptor (MR). To assess the potential role of GPR30 in mediating the effects of aldosterone and estradiol, GPR30 was re-introduced, since these cells lose endogenous GPR30 expression in culture. Re-expression of GPR30 enhanced both estradiol- and aldosterone-mediated contraction. These studies demonstrate that in rat aortic vascular smooth muscle cells, both aldosterone and estradiol mediate vascular smooth muscle contraction and that these effects can be mediated by MR, ERα, and by GPR30.

Glucocorticoids increase Ca2+ uptake and [3H]dihydropyridine binding in A7r5 vascular smooth muscle cells

1991 ◽  
Vol 261 (1) ◽  
pp. C106-C114 ◽  
Author(s):  
T. Hayashi ◽  
T. Nakai ◽  
S. Miyabo
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Binding Sites ◽  
Control Level ◽  
Muscle Cells ◽  
Calcium Handling ◽  
Dependent Manner

Increased levels of corticosteroids result in the development of hypertension in vivo. To investigate whether corticosteroids modulate calcium handling in vascular smooth muscle cells, we studied 45Ca2+ uptake and binding of [methyl-3H]PN 200-110, a potent dihydropyridine Ca2+ antagonist, in A7r5 vascular smooth muscle cells. Forty-eight-hour treatment with 100 nM dexamethasone increased the unidirectional 45Ca2+ uptake during a 2-min period, and the 30-min 45Ca2+ uptake of dexamethasone-treated cells was 95% greater than that of nontreated cells. The lag time for the dexamethasone effect on Ca2+ uptake was approximately 8 h. The effect of dexamethasone was blocked by the glucocorticoid antagonist RU 38486, whereas it was not affected by the mineralocorticoid antagonist RU 26752. After cessation of the dexamethasone treatment, 45Ca2+ uptake returned to the control level by 24 h. The effect of dexamethasone was completely blocked by nifedipine in a dose-dependent manner. Scatchard plots of [methyl-3H]PN 200-110 binding revealed two binding sites (Kd; 0.02 and 1 nM), and dexamethasone increased the number of the higher affinity binding sites. These results indicate that glucocorticoids increase Ca2+ uptake possibly mediated by an increase in the number of dihydropyridine-sensitive Ca2+ channels.

scholarly journals Translocon closure to Ca2+ leak in proliferating vascular smooth muscle cells

2009 ◽  
Vol 296 (4) ◽  
pp. H910-H916 ◽  
Author(s):  
Mohamed S Amer ◽  
Jing Li ◽  
David J. O'Regan ◽  
Derek S. Steele ◽  
Karen E. Porter ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Calcium Release ◽  
Calcium Ionophore ◽  
Muscle Cells ◽  
Calcium Handling ◽  
Leak Pathway

Vascular smooth muscle cells have a proliferative phenotype that is important in vascular development, adaptation, and disease. Intracellular calcium handling is thought to play pivotal roles in determining the properties of these cells, and thus previously unrecognized mechanisms for transmembrane calcium movement are of potential interest. An unsolved question is the mechanism of constitutive (passive) calcium leak from the intracellular stores. Studies of other cell types have suggested that the translocon is a calcium leak pathway. Here we investigated the contribution of the translocon in proliferating vascular smooth muscle cells. Calcium leak into the cytoplasm was measured using fura-2, and protein synthesis was measured using radioactive methionine. Puromycin, emetine, and anisomycin are chemicals that inhibit protein synthesis, acting via the translocon; all three agents strongly inhibited protein synthesis in the smooth muscle cells within 1 h. Puromycin, which opens the translocon, evoked a transient increase in cytoplasmic calcium that was similar in amplitude to the calcium rise evoked by thapsigargin. The puromycin effect was abolished by thapsigargin. The treatment of cells for 1 h with emetine or anisomycin, which close the translocon, inhibited the calcium release evoked by puromycin but not the calcium release evoked by extracellular ATP, endothelin-1, or the calcium ionophore ionomycin. Thapsigargin-evoked calcium rises were slightly suppressed by emetine but unaffected by puromycin or anisomycin. The data suggest that the translocon has the capacity to act as a calcium leak pathway in the ribosomal endoplasmic reticulum but that it is normally closed and lacks relevance to physiological calcium leak mechanisms.

Activated mineralocorticoid receptor regulates micro‐RNA‐29b in vascular smooth muscle cells

2016 ◽  
Vol 30 (4) ◽  
pp. 1610-1622 ◽  
Author(s):  
Maria Bretschneider ◽  
Bianca Busch ◽  
Daniel Mueller ◽  
Alexander Nolze ◽  
Barbara Schreier ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Mineralocorticoid Receptor ◽  
Muscle Cells ◽  
Micro Rna
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