No abstract available.
Angiotensins ; Muscle, Smooth ; Myocytes, Smooth Muscle

Glomus tumors are benign neoplasms that are derived from modified smooth muscle cells known as glomus cells. Histologically, it can be subdivided as glomus tumor proper, glomangioma, and glomangiomyoma according to relative proportions of components. Glomangiomyomas are the least frequent type and their overall architectural pattern may resemble glomus tumor proper or glomangioma, but there is a gradual transition from glomus cells to elongated mature smooth muscle cells. This transition is most obvious in the region surrounding large vessels. We present a case of glomangiomyoma of the left upper arm and the left fourth finger, in which ten-year history of two painful, bluish-colored subcutaneous nodules. On histologic examination, this case showed marked smooth muscle cell proliferation around large vessles and mucinous stromal change.
Arm ; Fingers ; Glomus Tumor ; Mucins* ; Muscle, Smooth* ; Myocytes, Smooth Muscle*

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

We demonstrated the effect of nortriptyline, a tricyclic antidepressant drug and serotonin reuptake inhibitor, on voltage-dependent K⁺ (Kv) channels in freshly isolated rabbit coronary arterial smooth muscle cells using a whole-cell patch clamp technique. Nortriptyline inhibited Kv currents in a concentration-dependent manner, with an apparent IC₅₀ value of 2.86±0.52 µM and a Hill coefficient of 0.77±0.1. Although application of nortriptyline did not change the activation curve, nortriptyline shifted the inactivation current toward a more negative potential. Application of train pulses (1 or 2 Hz) did not change the nortriptyline-induced Kv channel inhibition, suggesting that the effects of nortiprtyline were not use-dependent. Preincubation with the Kv1.5 and Kv2.1/2.2 inhibitors, DPO-1 and guangxitoxin did not affect nortriptyline inhibition of Kv channels. From these results, we concluded that nortriptyline inhibited Kv channels in a concentration-dependent and state-independent manner independently of serotonin reuptake.
Coronary Vessels ; Muscle, Smooth* ; Myocytes, Smooth Muscle* ; Nortriptyline* ; Serotonin

In this study, we demonstrated the inhibitory effect of the Class Ic antiarrhythmic agent propafenone on voltage-dependent K⁺ (Kv) channels using freshly isolated coronary artery smooth muscle cells from rabbits. The Kv current amplitude was progressively inhibited by propafenone in a dose-dependent manner, with an apparent IC₅₀ value of 5.04±1.05 µM and a Hill coefficient of 0.78±0.06. The application of propafenone had no significant effect on the steady-state activation and inactivation curves, indicating that propafenone did not affect the voltage-sensitivity of Kv channels. The application of train pulses at frequencies of 1 or 2 Hz progressively increased the propafenone-induced inhibition of the Kv current. Furthermore, the inactivation recovery time constant was increased after the application of propafenone, suggesting that the inhibitory action of propafenone on Kv current is partially use-dependent. Pretreatment with Kv1.5, Kv2.1 or Kv7 inhibitor did not change the inhibitory effect of propafenone on the Kv current. Together, these results suggest that propafenone inhibits the vascular Kv channels in a dose- and use-dependent manner, regardless of Na⁺ channel inhibition.
Coronary Vessels ; Muscle, Smooth* ; Myocytes, Smooth Muscle* ; Propafenone* ; Rabbits

We investigated the inhibitory effect of escitalopram, a selective serotonin reuptake inhibitor (SSRI), on voltage-dependent K⁺ (Kv) channels in freshly separated from rabbit coronary arterial smooth muscle cells. The application of escitalopram rapidly inhibited vascular Kv channels. Kv currents were progressively inhibited by an increase in the concentrations of escitalopram, suggesting that escitalopram inhibited vascular Kv currents in a concentration-dependent manner. The IC₅₀ value and Hill coefficient for escitalopram-induced inhibition of Kv channels were 9.54±1.33 µM and 0.75±0.10, respectively. Addition of escitalopram did not alter the steady-state activation and inactivation curves, suggesting that the voltage sensors of the channels were not affected. Pretreatment with inhibitors of Kv1.5 and/or Kv2.1 did not affect the inhibitory action of escitalopram on vascular Kv channels. From these results, we concluded that escitalopram decreased the vascular Kv current in a concentration-dependent manner, independent of serotonin reuptake inhibition.
Citalopram* ; Coronary Vessels ; Muscle, Smooth* ; Myocytes, Smooth Muscle* ; Serotonin*

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

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

Cutaneous piloleiomyomas are benign smooth muscle tumors arising from the arrector pili muscles. Piloleiomyomas appear as firm dermal papules of skin color or with a reddish to brown surface, and are commonly located on the extremities. Histologically, these lesions are composed of interlacing bundles of smooth muscle cells in the reticular dermis. Our case presented with an unusually large nodule on the forehead that was accompanied by intermittent pain. Histological analysis was compatible with piloleiomyoma and the lesion showed haphazardly arranged bundles of smooth muscle in the dermis. We describe herein an interesting case of a giant piloleiomyoma occurring on the forehead.
Dermis ; Extremities ; Forehead ; Muscle, Smooth ; Muscles ; Myocytes, Smooth Muscle ; Skin ; Smooth Muscle Tumor

BACKGROUND: The contraction of smooth muscle depends on an increase in the concentration of intracellular calcium ion and the source of this increase to various stimuli is different according to organs or species. Nevertheless, there have been only a few studies on human stomach smooth muscle. This study was designed to identify the source of the calcium utilized in the muscle contraction induced by carbachol, which is an important factor among various stimuli. METHODS: After the administration of carbachol with various conditions in cultured human stomach smooth muscle cells, fura-2-acetoxymethyl ester was used to measure the increase in the intracellular calcium concentration. RESULTS: (1) The carbachol-induced increase in the intracellular calcium concentration was not attenuated after removal of extracellular calcium. (2) Carbachol induced a small increase in the intracellular calcium concentration even after the depletion of intracellular calcium store. (3) Repeated histamine administration blocked the carbachol-induced increase in the intracellular calcium concentration in calcium-free extracellular solution. CONCLUSION: The main source of calcium utilized in human stomach smooth muscle contraction by carbachol is intracellular calcium store, particularly inositol triphosphate(IP3)-sensitive calcium stores. However, extracellular calcium also contributes to the carbachol-induced increase in the intracellular calcium concentration.
Calcium* ; Carbachol* ; Histamine ; Humans* ; Inositol ; Muscle Contraction ; Muscle, Smooth* ; Myocytes, Smooth Muscle* ; Stomach