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

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

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

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 smooth muscle cell (vSMC) is the predominant cell type in the blood vessel wall and is constantly subjected to a complex extracellular microenvironment. Mechanical forces that are conveyed by changes in stiffness/elasticity, geometry and topology of the extracellular matrix have been indicated by experimental studies to affect the phenotype and function of vSMCs. vSMCs perceive the mechanical stimuli from matrix via specialized mechanosensors, translate these stimuli into biochemical signals controlling gene expression and activation, with the consequent modulation in controlling various aspects of SMC behaviors. Changes in vSMC behaviors may further cause disruption of vascular homeostasis and then lead to vascular remodeling. A better understanding of how SMC senses and transduces mechanical forces and how the extracellular mechano-microenvironments regulate SMC phenotype and function may contribute to the development of new therapeutics for vascular diseases.
Biophysics ; Cells, Cultured ; Extracellular Matrix ; Humans ; Muscle, Smooth, Vascular ; Myocytes, Smooth Muscle ; Phenotype ; Vascular Remodeling

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*