scholarly journals Hydrogen peroxide influence on contractile activity smooth muscle cells: the role of cytoskeleton

2009 ◽  
Vol 8 (4) ◽  
pp. 41-46
Author(s):  
I. V. Kovalyev ◽  
S. V. Gusakova ◽  
O. S. Melnik ◽  
M. B. Baskakov ◽  
L. V. Kapilevich ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Contractile Activity ◽  
Smooth Muscles ◽  
Potassium Conductance ◽  
Muscle Cells ◽  
Rat Aorta ◽  
Mechanisms Of Action

The influence of of hydrogen peroxide on the contractile reactions of smooth muscle cells caused by hyperpotassium solution end phenylephrine in modulation a potassium conductance the membrane and the state of cytoskeleton elements has been investigated by the mechanographical method. It has multidirectional influence of hydrogen peroxide in the reduction of smooth muscles of rat aorta with the membrane depolarization hyperpotassium solution and action phenylephrine: phenylephrine decline in value and increase strength hyperpotassium contractures. We show that the cytoskeleton components involved in the mechanisms of action of hydrogen peroxide in the contractile reactions of smooth muscles of rat aorta caused by phenylephrine.

scholarly journals Mechanisms of regulation electric and contractile activity smooth muscle cells: the role of cytoskeleton

2008 ◽  
Vol 7 (4) ◽  
pp. 31-37
Author(s):  
M. A. Medvedev ◽  
M. B. Baskakov ◽  
S. V. Gusakova ◽  
I. V. Kovalyov ◽  
O. S. Melnik ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Smooth Muscle Cells ◽  
Contractile Activity ◽  
Smooth Muscles ◽  
Muscle Cells ◽  
Mechanisms Of Action ◽  
Electric Stimulus ◽  
Cytochalasine B

The influence of modulation of cytoskeleton by colchicine, vinblastine, cytochalasine B and docetaxel on contractile reactions of smooth muscle cells caused by electric stimulus, depolarization, phenylephrine has been investigated by the mechanographical method, by the methods of the double sucrose gup junction. It is established, that induced by a isoosmotic hyperpotassium solution of reduction of smooth muscle of the rat’s aorta, and also caused depolarization stimulus potentials of action and reductions smooth muscle cells from guinea pig urethra, depend more on the condition of microfilaments cytoskeleton than on microtubules. The reduction of smooth muscles cells of an aorta of the rat, caused by isoosmotic striction, is suppressed under the destruction microfilaments whereas the reduction in a hyperosmotic solution depends on a condition of both microfilaments, and microtubules. Cytoskeleton’s microfilaments of aorta’s smooth muscles and microtubules of smooth muscles of cells ureter are involved in mechanisms of action phenylephrine’s action on contractile activity of smooth muscle cells of an aorta and ureter.

scholarly journals Effect of hydrogen sulfide on the contractile activity of smooth muscle cells from the rat aorta

2010 ◽  
Vol 9 (6) ◽  
pp. 12-17
Author(s):  
M. B. Baskakov ◽  
S. V. Gusakova ◽  
A. S. Zheludeva ◽  
L. V. Smagly ◽  
I. V. Kovalyov ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Hydrogen Sulfide ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Contractile Activity ◽  
Muscle Cells ◽  
Rat Aorta ◽  
Mechanisms Of Action ◽  
High K ◽  
Lower Amplitude

In preparations of rat aorta, used as a model of muscular type arteries, the method mehanografii studied the effect of hydrogen sulfide on the reduction of isolated of vascular smooth muscle. Found that hydrogen sulfide in concentrations 1—50 mmol increases the mechanical stress of smooth muscle in high-K + medium. At higher concentrations (300—1 000 mmol) H2S leads to lower amplitude giperkalievoy contraction in high-K + medium. Reduction of smooth muscle cells caused by phenylephrine inhibited the action of hydrogen sulfide in the whole range of concentrations. The causes of differences in data obtained with the results of studies in other laboratories, and possible mechanisms of action of hydrogen sulfide on the contractile activity of vascular smooth muscle.

scholarly journals Role of nitric oxide and cytoskeleton in regulation of contractile activity smooth muscle cells

2009 ◽  
Vol 8 (3) ◽  
pp. 17-22
Author(s):  
S. V. Gusakova ◽  
M. B. Baskakov ◽  
I. V. Kovalev ◽  
O. S. Melnik ◽  
L. V. Kapilevich ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Sodium Nitroprusside ◽  
Contractile Activity ◽  
Muscle Cells ◽  
Rat Aorta

The influence of modulation of cytoskeleton by colchicine, nocodazole and cytochalasine D on contractile reactions of smooth muscle cells caused by depolarization, phenylephrine end sodium nitroprusside has been investigated by the mechanographical method. It was found that the reduction in smooth muscle cells of rat aorta caused by fenilefrin more sensitive to sodium nitroprusside than the reduction induced hyperpotassium solution. We show that microtubules involved in relaxation, indirect nitric oxide of smooth muscle in hyperpotassium solution, whereas the efficiency of relaxing influence of nitric oxide in rat aorta smooth muscle in the action depends on phenylephrine and microfilaments and microtubules.

scholarly journals The Role of Two-Pore Channels in Norepinephrine-Induced [Ca2+]i Rise in Rat Aortic Smooth Muscle Cells and Aorta Contraction

Cells ◽  
2019 ◽  
Vol 8 (10) ◽  
pp. 1144 ◽  
Author(s):  
Sergei K. Trufanov ◽  
Elena Yu. Rybakova ◽  
Piotr P. Avdonin ◽  
Alexandra A. Tsitrina ◽  
Irina L. Zharkikh ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Calcium Concentration ◽  
Muscle Cells ◽  
Rat Aorta ◽  
Structural Analogue ◽  
Aortic Smooth Muscle ◽  
Cis And Trans ◽  
High Degree

Second messenger nicotinic acid adenine dinucleotide phosphate (NAADP) triggers Ca2+ release via two-pore channels (TPCs) localized in endolysosomal vesicles. The aim of the present work is to evaluate the role of TPCs in the action of norepinephrine (NE), angiotensin II (AngII), vasopressin (AVP), and 5-hydroxytriptamine (5-HT) on free cytoplasmic calcium concentration ([Ca2+]i) in smooth muscle cells (SMCs) isolated from rat aorta and on aorta contraction. To address this issue, the NAADP structural analogue and inhibitor of TPCs, NED 19, was applied. We have demonstrated a high degree of colocalization of the fluorescent signals of cis-NED 19 and endolysosmal probe LysoTracker in SMCs. Both cis- or trans-NED 19 inhibited the rise of [Ca2+]i in SMCs induced by 100 μM NE by 50–60%. IC50 for cis- and trans-NED 19 were 2.7 and 8.9 μM, respectively. The inhibition by NED 19 stereoisomers of the effects of AngII, AVP, and 5-HT was much weaker. Both forms of NED 19 caused relaxation of aortic rings preconstricted by NE, with relative potency of cis-NED 19 several times higher than that of trans-NED 19. Inhibition by cis-NED 19 of NE-induced contraction was maintained after intensive washing and slowly reversed within an hour of incubation. Cis- and trans-NED 19 did not cause decrease in the force of aorta contraction in response to Ang II and AVP, and only slightly relaxed aorta preconstricted by 5-HT and by KCl. Suppression of TPC1 in SMCs with siRNA caused a 40% decrease in [Ca2+]i in response to NE, whereas siRNA against TPC2 did not change NE calcium signaling. These data suggest that TPC1 is involved in the NE-stimulated [Ca2+]i rise in SMCs. Inhibition of TPC1 activity by NED 19 could be the reason for partial inhibition of aortic rings contraction in response to NE.

Vasoconstriction: a new activity for platelet-derived growth factor

Science ◽  
1986 ◽  
Vol 232 (4746) ◽  
pp. 87-90 ◽  
Author(s):  
BC Berk ◽  
RW Alexander ◽  
TA Brock ◽  
MA Gimbrone ◽  
RC Webb
Keyword(s):  
Smooth Muscle ◽  
Growth Factor ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Rat Aorta ◽  
Platelet Derived Growth Factor ◽  
Free Calcium ◽  
Free Calcium Concentration ◽  
Cytosolic Free Calcium Concentration

Platelet-derived growth factor (PDGF) is a potent mitogen for vascular smooth muscle cells that has been implicated in the pathogenesis of atherosclerosis. The potential role of PDGF in the altered vasoreactivity of atherosclerotic vessels has been studied through an examination of its effects on contractility in the rat aorta. PDGF caused a concentration-dependent contraction of aortic strips and was significantly more potent on a molar basis than the classic vasoconstrictor peptide angiotensin II. Furthermore, PDGF increased the cytosolic free calcium concentration in cultured rat aortic smooth muscle cells. These observations suggest a new biological activity for PDGF that may contribute to the enhanced vasoreactivity of certain atherosclerotic vessels.

scholarly journals Interactions between A2A adenosine receptors, hydrogen peroxide, and KATP channels in coronary reactive hyperemia

2013 ◽  
Vol 304 (10) ◽  
pp. H1294-H1301 ◽  
Author(s):  
Maryam Sharifi-Sanjani ◽  
Xueping Zhou ◽  
Shinichi Asano ◽  
Stephen Tilley ◽  
Catherine Ledent ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Reactive Hyperemia ◽  
Katp Channels ◽  
Muscle Cells ◽  
Coronary Smooth Muscle ◽  
A2a Adenosine Receptors ◽  
Signaling Mechanisms

Myocardial metabolites such as adenosine mediate reactive hyperemia, in part, by activating ATP-dependent K+ (KATP) channels in coronary smooth muscle. In this study, we investigated the role of adenosine A2A and A2B receptors and their signaling mechanisms in reactive hyperemia. We hypothesized that coronary reactive hyperemia involves A2A receptors, hydrogen peroxide (H2O2), and KATP channels. We used A2A and A2B knockout (KO) and A2A/2B double KO (DKO) mouse hearts for Langendorff experiments. Flow debt for a 15-s occlusion was repaid 128 ± 8% in hearts from wild-type (WT) mice; this was reduced in hearts from A2A KO and A2A/2B DKO mice (98 ± 9 and 105 ± 6%; P < 0.05), but not A2B KO mice (123 ± 13%). Patch-clamp experiments demonstrated that adenosine activated glibenclamide-sensitive KATP current in smooth muscle cells from WT and A2B KO mice (90 ± 23% of WT) but not A2A KO or A2A/A2B DKO mice (30 ± 4 and 35 ± 8% of WT; P < 0.05). Additionally, H2O2 activated KATP current in smooth muscle cells (358 ± 99%; P < 0.05). Catalase, an enzyme that breaks down H2O2, attenuated adenosine-induced coronary vasodilation, reducing the percent increase in flow from 284 ± 53 to 89 ± 13% ( P < 0.05). Catalase reduced the repayment of flow debt in hearts from WT mice (84 ± 9%; P < 0.05) but had no effect on the already diminished repayment in hearts from A2A KO mice (98 ± 7%). Our findings suggest that adenosine A2A receptors are coupled to smooth muscle KATP channels in reactive hyperemia via the production of H2O2 as a signaling intermediate.

scholarly journals Mechanism of vascular smooth muscle cells activation by hydrogen peroxide: role of phospholipase C gamma

2002 ◽  
Vol 17 (3) ◽  
pp. 392-398 ◽  
Author(s):  
Francisco R. González‐Pacheco ◽  
Carlos Caramelo ◽  
Maria Ángeles Castilla ◽  
Juan J. P. Deudero ◽  
Javier Arias ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Phospholipase C ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Phospholipase C Gamma

scholarly journals The role of K+ conductances in regulating membrane excitability in human gastric corpus smooth muscle

2015 ◽  
Vol 308 (7) ◽  
pp. G625-G633 ◽  
Author(s):  
Ji Yeon Lee ◽  
Eun-ju Ko ◽  
Ki Duck Ahn ◽  
Sung Kim ◽  
Poong-Lyul Rhee
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Smooth Muscles ◽  
Muscle Cells ◽  
Bk Channels ◽  
Resting Membrane Potential ◽  
Membrane Excitability ◽  
Gastric Corpus ◽  
Isolated Smooth Muscle Cells

Changes in resting membrane potential (RMP) regulate membrane excitability. K+ conductance(s) are one of the main factors in regulating RMP. The functional role of K+ conductances has not been studied the in human gastric corpus smooth muscles (HGCS). To examine the role of K+ channels in regulation of RMP in HGCS we employed microelectrode recordings, patch-clamp, and molecular approaches. Tetraethylammonium and charybdotoxin did not affect the RMP, suggesting that BK channels are not involved in regulating RMP. Apamin, a selective small conductance Ca2+-activated K+ channel (SK) blocker, did not show a significant effect on the membrane excitability. 4-Aminopyridine, a Kv channel blocker, caused depolarization and increased the duration of slow wave potentials. 4-Aminopyridine also inhibited a delayed rectifying K+ current in isolated smooth muscle cells. End-product RT-PCR gel detected Kv1.2 and Kv1.5 in human gastric corpus muscles. Glibenclamide, an ATP-sensitive K+ channel (KATP) blocker, did not induce depolarization, but nicorandil, a KATP opener, hyperpolarized HGCS, suggesting that KATP are expressed but not basally activated. Kir6.2 transcript, a pore-forming subunit of KATP was expressed in HGCS. A low concentration of Ba2+, a Kir blocker, induced strong depolarization. Interestingly, Ba2+-sensitive currents were minimally expressed in isolated smooth muscle cells under whole-cell patch configuration. KCNJ2 (Kir2.1) transcript was expressed in HGCS. Unique K+ conductances regulate the RMP in HGCS. Delayed and inwardly rectifying K+ channels are the main candidates in regulating membrane excitability in HGCS. With the development of cell dispersion techniques of interstitial cells, the cell-specific functional significance will require further analysis.

The role of intracellular Ca2+ pool in sodium nitroprusside-induced relaxation of rat aorta smooth muscle cells

1999 ◽  
Vol 127 (2) ◽  
pp. 160-162 ◽  
Author(s):  
I. V. Kovalev ◽  
M. B. Baskakov ◽  
L. V. Kapilevich ◽  
M. A. Medvedev ◽  
A. A. Panov ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Sodium Nitroprusside ◽  
Muscle Cells ◽  
Rat Aorta
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