No abstract available.
Cytosol* ; Muscle, Smooth, Vascular*

No abstract available.
Lipoproteins* ; Muscle, Smooth, Vascular*

BACKGROUND: Midazolam has a direct relaxing effect on vascular smooth muscle, but the mechanisms that this agent produces muscle relaxation are not fully understood. The current study was performed to identify the effects of the midazolam on K+ channels current in rabbit cerebral arterial smooth muscle cells. METHODS: Whole cell patch-clamp recording technique was used to evaluate the effects of midazolam (0.1 to 100micrometer) on outward K+ channel currents in dispersed rabbit cerebral arterial smooth muscle cells. RESULTS: Outward K+ currents of rabbit cerebral artery smooth muscle cells were voltage-dependent. Midazolam (10, 100micrometer) tested significantly inhibited outward K+ currents in a dose-dependent manner and half-blocking concentration (IC50) was 15.94micrometer at 60 mV. CONCLUSIONS: Midazolam inhibit outward K+ currents of rabbit cerebral arterial smooth muscle cells. Further study will be needed to determine the effect of midazolam on calcium channel current because it is unclear if the inhibitory effect of midazolam on outward K+current induces vasoconstriction.
Calcium Channels ; Cerebral Arteries ; Midazolam* ; Muscle Relaxation ; Muscle, Smooth* ; Muscle, Smooth, Vascular ; Myocytes, Smooth Muscle* ; Vasoconstriction

Humans ; MicroRNAs ; Muscle, Smooth, Vascular ; Myocytes, Smooth Muscle ; Phenotype

No abstract available.
Chemokine CCL2* ; Humans* ; Monocytes* ; Muscle, Smooth, Vascular*

No abstract available.
Animals ; Muscle, Smooth, Vascular* ; Nitric Oxide* ; Rats*

No abstract available.
MicroRNAs* ; Myocytes, Smooth Muscle* ; Vascular Diseases*

The Kv channel activity in vascular smooth muscle cell plays an important role in the regulation of membrane potential and blood vessel tone. It was postulated that increased blood vessel tone in hypertension was associated with alteration of Kv channel and membrane potential. Therefore, using whole cell mode of patch-clamp technique, the membrane potential and the 4-AP-sensitive Kv current in cerebral arterial smooth muscle cells were compared between normotensive rat and one-kidney, one-clip Goldblatt hypertensive rat (1K,1C-GBH rat). Cell capacitance of hypertensive rat was similar to that of normotensive rat. Cell capacitance of normotensive rat and 1K,1C-GBH rat were 20.8+/-2.3 and 19.5+/-1.4 pF, respectively. The resting membrane potentials measured in current clamp mode from normotensive rat and 1K,1C-GBH rat were -45.9+/-1.7 and -38.5+/-1.6 mV, respectively. 4-AP (5 mM) caused the resting membrane potential hypopolarize but charybdotoxin (0.1 muM) did not cause any change of membrane potential. Component of 4-AP-sensitive Kv current was smaller in 1K,1C-GBH rat than in normotensive rat. The voltage dependence of steady-state activation and inactivation of Kv channel determined by using double-pulse protocol showed no significant difference. These results suggest that 4-AP-sensitive Kv channels play a major role in the regulation of membrane potential in cerebral arterial smooth muscle cells and alterations of 4-AP-sensitive Kv channels would contribute to hypopolarization of membrane potential in 1K,1C-GBH rat.
Animals ; Blood Vessels ; Charybdotoxin ; Hypertension ; Membrane Potentials ; Muscle, Smooth* ; Muscle, Smooth, Vascular ; Myocytes, Smooth Muscle* ; Patch-Clamp Techniques ; Rats*

Vascular calcification, the deposition of calcium in the arterial wall, is often linked to increased stiffness of the vascular wall. Vascular calcification is one of the important factors for high morbidity and mortality of cardiovascular and cerebrovascular diseases, as well as an important biomarker in atherosclerotic cardiovascular events, stroke and peripheral vascular diseases. The mechanism of vascular calcification has not been fully elucidated. Recently, non-coding RNAs have been found to play an important role in the process of vascular calcification. In this paper, the main types of non-coding RNAs and their roles involved in vascular smooth muscle cell calcification are reviewed, including the changes of osteoblast-related proteins, calcification signaling pathways and intracellular Ca²⁺.
Humans ; Muscle, Smooth, Vascular/metabolism* ; Vascular Calcification/metabolism* ; Myocytes, Smooth Muscle/metabolism*

Vascular calcification is an important pathophysiological basis of cardiovascular disease with its underlying mechanism unclear. In recent years, studies have shown that aging is one of the risk factors for vascular calcification. The purpose of this study was to investigate the microenvironmental characteristics of vascular calcification, identify aging/senescence-induced genes (ASIGs) closely related to calcified plaques, and explore the evolution trajectory of vascular calcification cell subsets. Based on the bioinformatics method, the single cell transcriptome sequencing data (Gene Expression Omnibus: GSE159677) of carotid artery samples from 3 patients undergoing carotid endarterectomy were grouped and annotated. Vascular calcification-related aging genes were identified by ASIGs data set. The pseudotime trend of ASIGs in cell subsets was analyzed by Monocle 3, and the evolution of vascular calcification cells was revealed. After quality control, all cells were divided into 8 cell types, including B cells, T cells, smooth muscle cells, macrophages, endothelial cells, fibroblasts, mast cells, and progenitor cells. Ten ASIGs related to vascular calcification were screened from the data set of ASIGs, which include genes encoding complement C1qA (C1QA), superoxide dismutase 3 (SOD3), lysozyme (LYZ), insulin-like growth factor binding protein-7 (IGFBP7), complement C1qB (C1QB), complement C1qC (C1QC), Caveolin 1 (CAV1), von Willebrand factor (vWF), clusterin (CLU), and αB-crystallin (CRYAB). Pseudotime analysis showed that all cell subsets were involved in the progression of vascular calcification, and these ASIGs may play an important role in cell evolution. In summary, AGIS plays an important role in the progression of vascular calcification, and these high expression genes may provide ideas for early diagnosis and treatment of vascular calcification.
Humans ; Endothelial Cells ; Muscle, Smooth, Vascular ; Aging ; Vascular Calcification/metabolism* ; Computational Biology ; Myocytes, Smooth Muscle/metabolism*