scholarly journals Endurance exercise training restores atrophy-induced decreases of myogenic response and ionic currents in rat skeletal muscle artery

2019 ◽  
Vol 126 (6) ◽  
pp. 1713-1724 ◽  
Author(s):  
Ming Zhe Yin ◽  
Hae Jin Kim ◽  
Eun Yeong Suh ◽  
Yin Hua Zhang ◽  
Hae Young Yoo ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Exercise Training ◽  
Smooth Muscles ◽  
Ionic Currents ◽  
Myogenic Response ◽  
Mrna Levels ◽  
Voltage Gated ◽  
The Impact ◽  
Inwardly Rectifying ◽  
Channel Currents

Atrophic limbs exhibit decreased blood flow and histological changes in the arteries perfusing muscles. However, the effect of atrophy on vascular smooth muscle function is poorly understood. Here, we investigated the effect of unilateral sciatic denervation on the myogenic response (MR) and the ionic currents in deep femoral artery (DFA) smooth muscles from Sprague-Dawley rats. Because denervated rats were capable of treadmill exercise (20 m/min, 30 min, 3 times/wk), the impact of exercise training on these effects was also assessed. Skeletal arteries were harvested 3 or 5 wk after surgery. Then skeletal arteries or myocytes were subjected to video analysis of pressurized artery, myography, whole-cell patch clamp, and real-time quantitative PCR to determine the effect of hindlimb paralysis in the presence/absence of exercise training on MR, contractility, ionic currents, and channel transcription, respectively. In sedentary rats, atrophy was associated with loss of MR in the DFA at 5 wk. The contralateral DFA had a normal MR. At 5 wk after surgery, DFA myocytes from the atrophic limbs exhibited depressed L-type Ca2+currents, GTPγS-induced transient receptor potential cation channel (TRPC)-like currents, 80 mM KCl-induced vasoconstriction, TRPC6 mRNA, and voltage-gated K+and inwardly rectifying K+currents. Exercise training abrogated the differences in all of these functions between atrophic side and contralateral side DFA myocytes. These results suggest that a probable increase in hemodynamic stimuli in skeletal artery smooth muscle plays an important role in maintaining MR and ionic currents in skeletal artery smooth muscle. This may also explain the observed benefits of exercise in patients with limb paralysis.NEW & NOTEWORTHY Myogenic responses (MRs) in rat skeletal arteries feeding the unilateral atrophic hindlimb were impaired. In addition, the L-type Ca2+channel current, the TRPC6-like current, and TRPC6 mRNA levels in the corresponding myocytes decreased. Voltage-gated K+channel currents and inwardly rectifying K+channel currents were also attenuated in atrophic side myocytes. Exercise training effectively abrogated electrophysiological dysfunction of atrophic side myocytes and prevented loss of the MR.

Plasticity of KIR channels in human smooth muscle cells from internal thoracic artery

2003 ◽  
Vol 284 (6) ◽  
pp. H2325-H2334 ◽  
Author(s):  
Tom Karkanis ◽  
Shaohua Li ◽  
J. Geoffrey Pickering ◽  
Stephen M. Sims
Keyword(s):  
Smooth Muscle ◽  
Current Density ◽  
Internal Thoracic Artery ◽  
Smooth Muscles ◽  
Vascular Smooth Muscles ◽  
Rt Pcr ◽  
Regulation Of Proliferation ◽  
Negative Membrane Potential ◽  
Inwardly Rectifying ◽  
Contractile Cells

Inwardly rectifying K+ (KIR) currents are present in some, but not all, vascular smooth muscles. We used patch-clamp methods to examine plasticity of this current by comparing contractile and proliferative phenotypes of a clonal human vascular smooth muscle cell line. Hyperpolarization of cells under voltage clamp elicited a large inward current that was selective for K+ and blocked by Ba2+. Current density was greater in proliferative compared with contractile cells (−4.5 ± 0.9 and −1.4 ± 0.3 pA/pF, respectively; P < 0.001). RT-PCR of mRNA from proliferative cells identified transcripts for Kir2.1 and Kir2.2 but not Kir2.3 potassium channels. Western blot analysis demonstrated greater expression of Kir2.1 protein in proliferative cells, consistent with the higher current density. Proliferative cells displayed a more negative membrane potential than contractile cells (−71 ± 2 and −35 ± 4 mV, respectively; P < 0.001). Ba2+ depolarized all cells, whereas small increases in extracellular K+ concentration elicited hyperpolarization only in contractile cells. Ba2+ inhibited [3H]thymidine incorporation, indicating a possible role for KIR channels in the regulation of proliferation. The phenotype-dependent plasticity of KIR channels may have relevance to vascular remodeling.

A-type potassium currents in smooth muscle

2003 ◽  
Vol 284 (3) ◽  
pp. C583-C595 ◽  
Author(s):  
Gregory C. Amberg ◽  
Sang Don Koh ◽  
Yuji Imaizumi ◽  
Susumu Ohya ◽  
Kenton M. Sanders
Keyword(s):  
Smooth Muscle ◽  
Physiological Function ◽  
Smooth Muscles ◽  
Cell Types ◽  
Cardiac Cell ◽  
Biophysical Properties ◽  
Voltage Gated ◽  
Gastrointestinal Smooth Muscle ◽  
Molecular Identity ◽  
Rapid Activation

A-type currents are voltage-gated, calcium-independent potassium (Kv) currents that undergo rapid activation and inactivation. Commonly associated with neuronal and cardiac cell-types, A-type currents have also been identified and characterized in vascular, genitourinary, and gastrointestinal smooth muscle cells. This review examines the molecular identity, biophysical properties, pharmacology, regulation, and physiological function of smooth muscle A-type currents. In general, this review is intended to facilitate the comparison of A-type currents present in different smooth muscles by providing a comprehensive report of the literature to date. This approach should also aid in the identification of areas of research requiring further attention.

Leptin induces a contracting effect on guinea pig tracheal smooth muscle via the Ob-R receptor mechanism: novel evidence

2020 ◽  
Vol 98 (11) ◽  
pp. 810-817
Author(s):  
Aamir Magzoub ◽  
Mohammed Al-Ayed ◽  
Ibrahim Ahmed Shaikh ◽  
Mohamed Shafiuddin Habeeb ◽  
Khalid Al-Shaibary ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Leptin Receptor ◽  
Smooth Muscles ◽  
Tracheal Smooth Muscle ◽  
Organ Bath ◽  
Data Acquisition Software ◽  
Passive Sensitization ◽  
The Impact

The purpose of this study was to explore the potential contracting effect of leptin on isolated guinea pig tracheal smooth muscle (TSM), the possible mechanism, and the impact of epithelium denudation or allergen sensitization, respectively. An in vitro experiment investigated the effect of leptin at a concentration of 250–1000 nmol/L on isolated guinea pig TSM with an intact or denuded epithelium. Ovalbumin and IgE were used to test the impact of active and passive sensitization. The isolated TSM strips were incubated in Krebs solution and aerated with carbogen (95% O2 and 5% CO2) via an automated tissue organ bath system (n = 4 for each group). Isometric contractions were recorded digitally using iox2 data acquisition software. The possible mechanism of leptin-induced TSM contraction was examined by preincubation with leptin receptor (Ob-R) antagonist. Leptin had significant concentration-dependent contraction effects on guinea pig TSM (p < 0.05). Epithelium denuding and active or passive sensitization significantly increased the potency of the leptin. Preincubation with a leptin receptor (Ob-R) antagonist significantly reduced the contraction effects, suggesting an Ob-R-mediated mechanism. Leptin had a contracting effect on airway smooth muscles potentiated by either epithelium denuding or sensitization, and the Ob-R mechanism was a possible effect mediator.

Classification of potassium and chlorine ionic currents in retinal ganglion cell line (RGC-5) by whole-cell patch clamp

2012 ◽  
Vol 29 (6) ◽  
pp. 275-282 ◽  
Author(s):  
SHU-JIE WANG ◽  
LAI-HUA XIE ◽  
BIN HENG ◽  
YAN-QIANG LIU
Keyword(s):  
Patch Clamp ◽  
Ion Channel ◽  
Ganglion Cell ◽  
Cell Line ◽  
Ionic Currents ◽  
Retinal Ganglion ◽  
Voltage Gated ◽  
Whole Cell Patch Clamp ◽  
Inwardly Rectifying

AbstractRetinal ganglion cell line (RGC-5) has been widely used as a valuable model for studying pathophysiology and physiology of retinal ganglion cells in vitro. However, the electrophysiological characteristics, especially a thorough classification of ionic currents in the cell line, remain to be elucidated in details. In the present study, we determined the resting membrane potential (RMP) in RGC-5 cell line and then identified different types of ionic currents by using the whole-cell patch-clamp technique. The RMP recorded in the cell line was between −30 and −6 mV (−17.6 ± 2.6 mV, n = 10). We observed the following voltage-gated ion channel currents: (1) inwardly rectifying Cl− current (ICl,ir), which could be blocked by Zn2+; (2) Ca2+-activated Cl− current (ICl,Ca), which was sensitive to extracellular Ca2+ and could be inhibited by disodium 4,4’-diisothiocyanatostilbene-2,2’-disulfonate; (3) inwardly rectifying K+ currents (IK1), which could be blocked by Ba2+; (4) a small amount of delayed rectifier K+ current (IK). On the other hand, the voltage-gated sodium channels current (INa) and transient outward potassium channels current (IA) were not observed in this cell line. These results further characterize the ionic currents in the RGC-5 cell line and are beneficial for future studies especially on ion channel (patho)physiology and pharmacology in the RGC-5 cell line.

scholarly journals Exercise training prevents Ca2+ dysregulation in coronary smooth muscle from diabetic dyslipidemic yucatan swine

2006 ◽  
Vol 101 (3) ◽  
pp. 752-762 ◽  
Author(s):  
Carol A. Witczak ◽  
Brian R. Wamhoff ◽  
Michael Sturek
Keyword(s):  
Smooth Muscle ◽  
Sarcoplasmic Reticulum ◽  
Exercise Training ◽  
Current Density ◽  
Treadmill Running ◽  
High Fat ◽  
Diabetic Dyslipidemia ◽  
Coronary Smooth Muscle ◽  
Voltage Gated ◽  
Channel Current

Aerobic exercise training is known to have profound cardioprotective effects in disease, yet cellular mechanisms remain largely undefined. We tested the hypothesis that increased sarcoplasmic reticulum Ca2+ buffering and increased voltage-gated Ca2+ channel density underlie coronary smooth muscle intracellular Ca2+ (Ca2+i) dysregulation in diabetic dyslipidemia and that exercise training would prevent these increases. Yucatan swine were maintained in 1) control, 2) alloxan-induced hyperglycemic, 3) high fat/cholesterol fed, 4) hyperglycemic plus high fat/cholesterol fed (diabetic dyslipidemic), and 5) diabetic dyslipidemic plus exercise-trained (treadmill running) conditions. After 20 wk, the heart was removed and smooth muscle cells isolated from the right coronary artery. We utilized fura-2 imaging of Ca2+i levels to separate the functional role of the sarcoendoplasmic reticulum Ca2+-ATPase (SERCA) from the Na+-Ca2+ exchanger and the plasmalemmal Ca2+-ATPase, and whole-cell patch clamp to examine voltage-gated Ca2+ channel current density (i.e., Ca2+ influx). Results indicated that diabetic dyslipidemia impaired plasmalemmal Ca2+ efflux, increased basal Ca2+i levels, increased SERCA protein and sarcoplasmic reticulum Ca2+i buffering, and elicited an ∼50% decrease in voltage-gated Ca2+ channel current density. Exercise training concurrent with the diabetic dyslipidemic state restored plasmalemmal Ca2+ efflux, SERCA protein, sarcoplasmic reticulum Ca2+i buffering, and voltage-gated Ca2+ channel current density to control levels. Interestingly, basal Ca2+i levels were significantly lower in the exercise-trained group compared with control. Collectively, these results demonstrate a crucial role for exercise in the prevention of diabetic dyslipidemia-induced Ca2+i dysregulation.

scholarly journals On the Mechanisms Whereby Temperature Affects Excitation-Contraction Coupling in Smooth Muscle

2002 ◽  
Vol 119 (1) ◽  
pp. 93-104 ◽  
Author(s):  
Theodor V. Burdyga ◽  
Susan Wray
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Action Potential ◽  
Guinea Pigs ◽  
Smooth Muscles ◽  
Ionic Currents ◽  
Temperature Sensitive ◽  
Isolated Cells ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling

Moderate cooling of smooth muscle can modulate force production and may contribute to pathophysiological conditions, but the mechanisms underlying its effects are poorly understood. Interestingly, cooling increases force in rat ureter, but decreases it in guinea pigs. Therefore, this study used ureteric smooth muscle as a model system to elucidate the mechanisms of the effects of cooling on excitation-contraction coupling. Simultaneous recordings of force, intracellular [Ca2+], and electrical activity were made in intact ureter and ionic currents measured in isolated cells. The increase in force amplitude in rat ureter with cooling was found to be due to a significant increase in the duration of the Ca2+ transient. This in turn was due to a marked prolongation of the action potential. In guinea pigs, both these parameters were much less affected by cooling. Examination of membrane currents revealed that differences in ion channel contribution to the action potential underlie these differences. In particular, cooling potentiated Ca2+-activated Cl− currents, which are present in rat but not guinea pig ureteric smooth muscle, and prolonged the plateau of the action potential and Ca2+ entry. The force-Ca2+ relationship revealed that the increased duration of the Ca2+ transient was sufficient in the rat, but not in the guinea pig, to overcome kinetic lags produced in both species by cooling and potentiate force. Ca2+ entry and release processes were largely temperature-insensitive, but the rate of relaxation was very temperature-sensitive. Effects of cooling on myosin light chain phosphatase, confirmed in experiments using calyculin A, appear to be the predominant mechanisms affecting relaxation. Thus, smooth muscle is diverse in its response to temperature, even when experimental variables, such as the mode of stimulation, are removed. Although the biochemical and mechanical events accompanying contraction are likely to be affected in similar ways by temperature, differences in electrical events lead to subsequent differences in these processes between smooth muscles.

Electro-Chemo-Mechanical Modeling of the Artery Myogenic Response

2014 ◽  
Vol 1685 ◽  
Author(s):  
Yali Li ◽  
Nakhiah Goulbourne
Keyword(s):  
Smooth Muscle ◽  
Constitutive Model ◽  
Viscoelastic Model ◽  
Ionic Currents ◽  
Tissue Level ◽  
Myogenic Response ◽  
Elastic Recoil ◽  
Chemomechanical Coupling ◽  
Level Model ◽  
Nonlinear Viscoelastic Model

ABSTRACTActive contraction of smooth muscle results in the myogenic response and vasomotion of arteries, which adjusts the blood flow and nutrient supply of the organism. It involves coupled electrobiochemical and chemomechanical processes. This paper presents a new constitutive model to describe the myogenic response of the artery wall under different transmural pressures. The model includes two major components: a cell-level model for the electrobiochemical process, and a tissue-level model for the chemomechanical coupling. The electrochemical model is a lumped Hodgkin-Huxley-type cell membrane model for the nanoscopic ionic currents: calcium, sodium, and potassium. The calculated calcium concentration serves as input for the chemomechanical portion of the model; its molecular binding and the reactions with other enzymes cause the relative sliding of thin and thick filaments of the contractile unit. In the chemomechanical model, a new nonlinear viscoelastic model is introduced to describe the time varying behavior of the smooth muscle. Specifically, this model captures the filament overlap effect, active stress evolution, initial velocity, and elastic recoil in the media layer. Using the proposed constitutive model and a thin-walled equilibrium equation, the myogenic response is calculated for different transmural pressures. The integrated model is able to capture the pressure-diameter relationship incorporating fewer parameters than previous work and with clear physical meanings.

Nitric oxide induces phosphodiesterase 4B expression in rat pulmonary artery smooth muscle cells

2006 ◽  
Vol 290 (4) ◽  
pp. L747-L753 ◽  
Author(s):  
Cornelius J. Busch ◽  
Heling Liu ◽  
Amanda R. Graveline ◽  
Kenneth D. Bloch
Keyword(s):  
Gene Expression ◽  
Nitric Oxide ◽  
Smooth Muscle ◽  
Protein Kinase ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Dominant Negative ◽  
Mrna Levels ◽  
Dependent Manner ◽  
The Impact

Phosphodiesterases (PDE) metabolize cyclic nucleotides limiting the effects of vasodilators such as prostacyclin and nitric oxide (NO). In this study, DNA microarray techniques were used to assess the impact of NO on expression of PDE genes in rat pulmonary arterial smooth muscle cells (rPASMC). Incubation of rPASMC with S-nitroso-l-glutathione (GSNO) increased expression of a PDE isoform that specifically metabolizes cAMP (PDE4B) in a dose- and time-dependent manner. GSNO increased PDE4B protein levels, and rolipram-inhibitable PDE activity was 2.3 ± 1.0-fold greater in GSNO-treated rPASMC than in untreated cells. The soluble guanylate cyclase (sGC) inhibitor, 1H-[1,2,4]oxadiazolo[4,3,-a]quinoxalin-1-one, and the cAMP-dependent protein kinase inhibitor, H89, prevented induction of PDE4B gene expression by GSNO, but the protein kinase G (PKG) inhibitors, Rp-8-pCPT-cGMPs and KT-5823, did not. Incubation of rPASMC with IL-1β and tumor necrosis factor-α induced PDE4B gene expression, an effect that was inhibited by l- N6-(1-iminoethyl)lysine, an antagonist of NO synthase 2 (NOS2). The GSNO-induced increase in PDE4B mRNA levels was blocked by actinomycin D but augmented by cycloheximide. Infection of rPASMC with an adenovirus specifying a dominant negative cAMP response element binding protein (CREB) mutant inhibited the GSNO-induced increase of PDE4B gene expression. These results suggest that exposure of rPASMC to NO induces expression of PDE4B via a mechanism that requires cGMP synthesis by sGC but not PKG. The GSNO-induced increase of PDE4B gene expression is CREB dependent. These findings demonstrate that NO increases expression of a cAMP-specific PDE and provide evidence for a novel “cross talk” mechanism between cGMP and cAMP signaling pathways.

Sarcoplasmic reticulum Ca2+ uptake is impaired in coronary smooth muscle distal to coronary occlusion

2001 ◽  
Vol 281 (1) ◽  
pp. H223-H231 ◽  
Author(s):  
Cristine L. Heaps ◽  
Michael Sturek ◽  
Elmer M. Price ◽  
M. Harold Laughlin ◽  
Janet L. Parker
Keyword(s):  
Smooth Muscle ◽  
Sarcoplasmic Reticulum ◽  
Exercise Training ◽  
Coronary Occlusion ◽  
Smooth Muscles ◽  
Cyclopiazonic Acid ◽  
Coronary Smooth Muscle ◽  
Protein Levels ◽  
Chronic Occlusion ◽  
Plasmic Reticulum

After chronic occlusion, collateral-dependent coronary arteries exhibit alterations in both vasomotor reactivity and associated myoplasmic free Ca2+ levels that are prevented by chronic exercise training. We tested the hypotheses that coronary occlusion diminishes Ca2+ uptake by the sarcoplasmic reticulum (SR) and that exercise training would prevent impaired SR Ca2+ uptake. Ameroid constrictors were surgically placed around the proximal left circumflex (LCx) artery of female swine 8 wk before initiating 16-wk sedentary (pen confined) or exercise-training (treadmill run) protocols. Twenty-four weeks after Ameroid placement, smooth muscles cells were enzymatically dissociated from both the LCx and nonoccluded left anterior descending (LAD) arteries of sedentary and exercise-trained pigs, and myoplasmic free Ca2+ was studied using fura 2 microfluorometry. After the SR Ca2+ store was partially depleted with caffeine (5 mM), KCl-induced membrane depolarization produced a significant decrease in the time to half-maximal ( t ½) myoplasmic free Ca2+ accumulation in LCx versus LAD cells of sedentary pigs. Furthermore, inhibition of sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA; 10 μM cyclopiazonic acid) significantly reduced t ½ in cells isolated from the LAD but not from the LCx. Exercise training did not prevent the differences in t ½ myoplasmic free Ca2+ accumulation observed between LCx and LAD cells. Occlusion or exercise training did not alter SERCA protein levels. These results support our hypothesis of impaired SR Ca2+ uptake in coronary smooth muscle cells isolated distal to chronic occlusion. Impaired SR Ca2+ uptake was independent of SERCA protein levels and was not prevented by exercise training.

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