Utilization of Calcium Pools During Pharmaco or Electromechanical Coupling in Smooth Muscle

1975 ◽  
Vol 53 (4) ◽  
pp. 586-591 ◽  
Author(s):  
D. Bose ◽  
I. R. Innes
Keyword(s):  
Smooth Muscle ◽  
Isometric Contraction ◽  
Electromechanical Coupling ◽  
Sodium Pump ◽  
Muscle Cells ◽  
Slow Phase ◽  
High Potassium ◽  
Cat Spleen ◽  
Pharmacomechanical Coupling ◽  
Potassium Deprivation

Isometric contraction of cat spleen capsule due to noradrenaline had a fast and a slow phase. These phases were due to a tightly and a loosely bound (or extracellular) pool of calcium, respectively. Depolarization due to high potassium caused mainly a reduction of the slow phase. In sodium-loaded spleen strips recovering from potassium deprivation, the sodium pump is electrogenic and the muscle cells are probably hyperpolarized. In this situation also the slow phase of noradrenaline response is reduced. It is concluded that both depolarization and hyper-polarization affect the utilization of loosely bound calcium and that tightly bound calcium may be released during 'pharmacomechanical coupling' in splenic smooth muscle.

scholarly journals Agonist-induced isometric contraction of reconstituted smooth muscle fiber from cultured smooth muscle cells.

1999 ◽  
Vol 79 ◽  
pp. 56
Author(s):  
Kazuhiko Oishi ◽  
Yasushi Takeda ◽  
Kazuhiro Yamaura ◽  
Hiromi Takano-Ohmuro ◽  
Masaatsu K. Uchida
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Fiber ◽  
Isometric Contraction ◽  
Muscle Cells ◽  
Smooth Muscle Fiber ◽  
Cultured Smooth Muscle Cells

Potassium and the recovery of splenic capsular smooth muscle after cold storage

1976 ◽  
Vol 54 (3) ◽  
pp. 322-326
Author(s):  
D. Bose ◽  
I. R. Innes
Keyword(s):  
Smooth Muscle ◽  
Ambient Temperature ◽  
Cold Storage ◽  
Sodium Pump ◽  
Intracellular Sodium ◽  
Free Medium ◽  
Bathing Medium ◽  
Cat Spleen ◽  
Sodium And Potassium ◽  
Low Ambient Temperature

Cat spleen capsular smooth muscle, depleted of potassium and enriched with sodium by cold storage in a potassium free medium, relaxed and underwent transient reduction in responsiveness to noradrenaline when potassium was introduced into the bathing medium. Both these effects could be blocked by ouabain, lithium substitution for sodium or low ambient temperature, suggesting possible involvement of the sodium pump. In the continued presence of potassium, relaxation was maintained but sensitivity to noradrenaline increased, possibly due to restoration of normal intracellular sodium and potassium concentrations.

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.

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

Abstract P182: The Novel Perivascular Adipose Tissue Adipokine, Chemerin, Signals Through G i - and Calcium-Dependent Mechanisms

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
David J Ferland ◽  
Emma S Darios ◽  
Richard R Neubig ◽  
Benita Sjögren ◽  
Nguyen Truong ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Isometric Contraction ◽  
Kinase Inhibitor ◽  
Rho Kinase ◽  
Muscle Cells ◽  
Calcium Flux ◽  
Western Blots ◽  
Perivascular Adipose Tissue ◽  
Erk Mapk

Chemerin is an adipokine associated with inflammation, increased blood pressure, and may be a link between the pathologies of obesity and hypertension. We tested the hypothesis that chemerin-induced contraction of the vasculature occurs via the chemerin receptor and calcium flux in smooth muscle cells. Known mediators of the amplified arterial responsiveness seen in hypertension (L-type Ca 2+ channels, Src, and Rho kinase) were interrogated by isometric contraction of rat aortic rings in parallel with calcium kinetics of rat aortic smooth muscle cells. Western blots were also used to observe phosphorylation of Erk/MAPK. Chemerin-9 (nonapeptide of the chemerin S 157 isoform) caused a concentration-dependent contraction of isolated aorta (EC 50 100 nM) and elicited a concentration-dependent intracellular calcium response (EC 50 10 nM). Both calcium influx and isometric contraction, respectively, were reduced (units of “% of vehicle response”) by Pertussis toxin (G i inhibitor; 0±3% and 23±9%), verapamil (L-type Ca 2+ channel inhibitor; 38±20% and 23±4%), PP1 (Src inhibitor; 43±23% and 15±4%), and Y27632 (Rho Kinase inhibitor; 58±23% and 22±4%) but U73122 (PLC inhibitor) had little to no effect (71±31% and 71±12%). PD098059 (Erk/MAPK inhibitor) did not inhibit chemerin-9 induced contraction (117±19%) and phosphorylation did not change after chemerin-9 stimulation [1.12±0.14 (44 kDa) and 1.11±0.29 (42 kDa) fold-increase with chemerin-9 contraction compared to vehicle, p>0.05]. The chemerin receptor-selective antagonist CCX832 inhibited chemerin-9-induced calcium flux and aortic contraction and calcium flux (0.1±10.3% and 10±7%). These data support a chemerin-induced contractile mechanism in vascular smooth muscle that functions through the G i -linked chemerin receptor to activate L-type Ca 2+ channels, Src, and Rho kinase. There is mounting evidence linking chemerin to hypertension and this mechanism brings us one step closer to targeting chemerin as a unique form of therapy.

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