Electromechanical coupling in smooth-muscle cells of the ureter studied with the aid of phenothiazines

1984 ◽  
Vol 97 (4) ◽  
pp. 438-440 ◽  
Author(s):  
M. B. Baskakov ◽  
I. V. Kovalev ◽  
M. A. Medvedev ◽  
N. P. Larionov
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Electromechanical Coupling ◽  
Muscle Cells

scholarly journals Functional characterization of voltage-dependent Ca2+ channels in mouse pulmonary arterial smooth muscle cells: divergent effect of ROS

2013 ◽  
Vol 304 (11) ◽  
pp. C1042-C1052 ◽  
Author(s):  
Eun A. Ko ◽  
Jun Wan ◽  
Aya Yamamura ◽  
Adriana M. Zimnicka ◽  
Hisao Yamamura ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Function ◽  
Electromechanical Coupling ◽  
Functional Characterization ◽  
Muscle Cells ◽  
Pulmonary Vascular Disease ◽  
High K ◽  
Voltage Dependent ◽  
Inward Currents

Electromechanical coupling via membrane depolarization-mediated activation of voltage-dependent Ca2+ channels (VDCC) is an important mechanism in regulating pulmonary vascular tone, while mouse is an animal model often used to study pathogenic mechanisms of pulmonary vascular disease. The function of VDCC in mouse pulmonary artery (PA) smooth muscle cells (PASMC), however, has not been characterized, and their functional role in reactive oxygen species (ROS)-mediated regulation of vascular function remains unclear. In this study, we characterized the electrophysiological and pharmacological properties of VDCC in PASMC and the divergent effects of ROS produced by xanthine oxidase (XO) and hypoxanthine (HX) on VDCC in PA and mesenteric artery (MA). Our data show that removal of extracellular Ca2+ or application of nifedipine, a dihydropyridine VDCC blocker, both significantly inhibited 80 mM K+-mediated PA contraction. In freshly dissociated PASMC, the maximum inward Ca2+ currents were −2.6 ± 0.2 pA/pF at +10 mV (with a holding potential of −70 mV). Window currents were between −40 and +10 mV with a peak at −15.4 mV. Nifedipine inhibited currents with an IC50 of 0.023 μM, and 1 μM Bay K8644, a dihydropyridine VDCC agonist, increased the inward currents by 61%. XO/HX attenuated 60 mM K+-mediated increase in cytosolic free Ca2+ concentration ([Ca2+]cyt) due to Ca2+ influx through VDCC in PASMC. Exposure to XO/HX caused relaxation in PA preconstricted by 80 mM K+ but not in aorta and MA. In contrast, H2O2 inhibited high K+-mediated increase in [Ca2+]cyt and caused relaxation in both PA and MA. Indeed, RT-PCR and Western blot analysis revealed significantly lower expression of CaV1.3 in MA compared with PA. Thus our study characterized the properties of VDCC and demonstrates that ROS differentially regulate vascular contraction by regulating VDCC in PA and systemic arteries.

Oxygen induces electromechanical coupling in arteriolar smooth muscle cells: a role for L-type Ca2+ channels

1998 ◽  
Vol 274 (6) ◽  
pp. H2018-H2024 ◽  
Author(s):  
Donald G. Welsh ◽  
William F. Jackson ◽  
Steven S. Segal
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Electromechanical Coupling ◽  
Lucifer Yellow ◽  
Muscle Cells ◽  
Mechanical Responses ◽  
Arteriolar Wall ◽  
Cheek Pouches ◽  
Arteriolar Diameter ◽  
Ca2 Channels

We tested whether O2-induced vasomotor responses of arterioles correspond to changes in membrane potential ( E m) of cells in the arteriolar wall. The cheek pouches of anesthetized male hamsters were prepared for intravital microscopy and intracellular recording. Microelectrodes containing Lucifer yellow dye were used to label smooth muscle cells (SMC) or endothelial cells (EC) during arteriolar responses to O2. During low-[Formula: see text] superfusion (∼20 Torr; arteriolar diameter 55 ± 2 μm), E m of SMC and EC averaged −37 and −36 mV, respectively. High-[Formula: see text] superfusion (∼150 Torr) depolarized SMC (to −15 ± 1 mV) with vasoconstriction (to 24 ± 2 μm) and diameter cycled with E m of SMC during vasomotion. In contrast, the E m of EC did not change with [Formula: see text] nor during vasomotion, yet E m depolarized by 21 ± 2 mV when the extracellular K+ concentration ([K+]o) was raised to 55 mM. Superfusion with diltiazem (10 μM) or nifedipine (1 μM) abolished vasomotor and electrical responses to[Formula: see text] in SMC but did not eliminate depolarizations to elevated [K+]o. We conclude that, under physiological conditions, electrical and mechanical responses of arteriolar SMC to changes in[Formula: see text] are mediated through L-type Ca2+ channels without corresponding electrical activity in EC.

Mechanisms of coronary artery depolarization by uridine triphosphate

2001 ◽  
Vol 280 (6) ◽  
pp. H2545-H2553 ◽  
Author(s):  
Donald G. Welsh ◽  
Joseph E. Brayden
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Electromechanical Coupling ◽  
Reversal Potential ◽  
Muscle Cells ◽  
Coronary Resistance ◽  
Resistance Arteries ◽  
Coronary Smooth Muscle ◽  
Uridine Triphosphate ◽  
Inwardly Rectifying

We sought to define the basic mechanisms by which pyrimidine nucleotides constrict rat coronary resistance arteries. Uridine triphosphate (UTP) caused a dose-dependent constriction in coronary arteries stripped of endothelium. UTP also depolarized and increased cytosolic Ca2+ in coronary smooth muscle cells. Nisoldipine, an antagonist of voltage-operated Ca2+channels, blocked the rise in cytosolic Ca2+ and reduced UTP-induced vasoconstriction by ∼75% which suggests a prominent role for depolarization in this constrictor response. The ionic basis of UTP-induced depolarization was subsequently explored in coronary smooth muscle cells using whole-cell patch-clamp electrophysiology. In the absence of K+ and with CsCl in the pipette, UTP (40 μM) activated a sustained inwardly rectifying current (−0.66 ± 0.10 pA/pF at −60 mV). A 100 mM reduction in bath Na+ shifted the reversal potential of this current (from −2 ± 1 to −28 ± 4 mV) and reduced the magnitude (from −2.26 ± 0.61 to −0.51 ± 0.11 pA/pF). In addition to activating a depolarizing cation current, UTP inhibited hyperpolarizing outward currents. Specifically, UTP inhibited ATP-sensitive and voltage-dependent K+ currents yet had no effect on inwardly rectifying and Ca2+-activated K+ channels. This study indicates that electromechanical coupling is integral to pyrimidine-induced constriction in coronary resistance arteries.

Effect of nitro derivatives on electromechanical coupling in ureteral smooth muscle cells

2000 ◽  
Vol 129 (5) ◽  
pp. 455-457
Author(s):  
I. V. Kovalev ◽  
A. G. Popov ◽  
A. A. Panov ◽  
Yu. L. Borodin ◽  
L. V. Kapilevich ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Electromechanical Coupling ◽  
Muscle Cells ◽  
Nitro Derivatives

Immunogold localization of HMB-45 antigen in pulmonary lymphangiomyomatosis

1995 ◽  
Vol 53 ◽  
pp. 998-999
Author(s):  
J.M. Minda ◽  
E. Dessy ◽  
G. G. Pietra
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Room Temperature ◽  
Osmium Tetroxide ◽  
Muscle Cells ◽  
Ultrastructural Localization ◽  
Reproductive Age ◽  
Thin Sections ◽  
Smooth Muscle Proliferation ◽  
Hmb 45

Pulmonary lymphangiomyomatosis (PLAM) is a rare disease occurring exclusively in women of reproductive age. It involves the lungs, lymph nodes and lymphatic ducts. In the lungs, it is characterized by the proliferation of smooth muscle cells around lymphatics in the bronchovascular bundles, lobular septa and pleura The nature of smooth muscle proliferation in PLAM is still unclear. Recently, reactivity of the smooth muscle cells for HMB-45, a melanoma-related antigen has been reported by immunohistochemistry. The purpose of this study was the ultrastructural localization of HMB-45 immunoreactivity in these cells using gold-labeled antibodies.Lung tissue from three cases of PLAM, referred to our Institution for lung transplantation, was embedded in either Poly/Bed 812 post-fixed in 1% osmium tetroxide, or in LR White, without osmication. For the immunogold technique, thin sections were placed on Nickel grids and incubated with affinity purified, monoclonal anti-melanoma antibody HMB-45 (1:1) (Enzo Diag. Co) overnight at 4°C. After extensive washing with PBS, grids were treated with Goat-anti-mouse-IgG-Gold (5nm) (1:10) (Amersham Life Sci) for 1 hour, at room temperature.

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