Effect of low extracellular calcium on shortening velocity in isolated single smooth muscle cells

Warshaw, David M.; Work, Steven S.; McBride, Whitney

doi:10.1007/bf00581914

Cited by 5 publications

(7 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The rate of force development after stimulation was half the rate in normal extracellular calcium. In addition, at the peak of isometric force, both the maximum active stress and Young's modulus were ~35% of that in normal calcium, confirming our previous observations (Warshaw et al, 1987b).…”

Section: Extracellular Calcium: Effects On Force Development and Tenssupporting

confidence: 90%

“…Although the larger cell diameters in low extracellular calcium could be interpreted as swelling due to the change in extracellular calcium, we do not believe this is the case. In a previous study (Warshaw et al, 1987b), no difference in cell diameter was observed for cells in normal and low extraceilular calcium.…”

Section: Extracellular Calcium: Effects On Force Development and Tensmentioning

confidence: 66%

“…The attachment procedure, which required knotting the cell to the recording system under the microscope, was performed at room temperature in amphibian physiological saline (APS; Warshaw and Fay, 1983a) having either normal (1.8 mM) or low (0.18 mM) extracellular calcium. To tighten the knots at the ends of the cell, relaxed cells were stretched to a length (Lc~O at which a transient passive tension of ~0.2 #N was observed (Warshaw et al, 1987b). To activate the cell, transverse electric field stimulation was applied through platinum paddles (cross-sectional area, 0.2 mm2).…”

Section: Single-cell Preparation and Instrumentationmentioning

confidence: 99%

“…If the reduced maximum shortening velocity in low extracellular calcium (Warshaw et al, 1987b) is indicative of a slower crossbridge cycling rate, then one might expect corresponding reductions in the rate of tension recovery after a length step applied to cells exposed to low extracellular calcium. These tension recoveries in response to step-length changes were once again best described by the sum of two exponentials having rate constants of 40-130 s -~ for the fast recovery phase and 1-5 s -I for the slow phase.…”

Section: Extracellular Calcium: Effects On Force Development and Tensmentioning

confidence: 99%

“…When compared with fast skeletal muscle, smooth muscle contracts slower and generates comparable or greater stress (i.e., force per crosssectional area of muscle) but with far less myosin than in skeletal muscle (Cohen and Murphy, 1979). In addition, the maximum velocity of shortening in smooth muscle can be modulated by changes in extracellular calcium (Warshaw et al, 1987b;Siegman et al, 1984). These mechanical characteristics may reflect inherent differences in the crossbridge cycle of smooth muscle relative to skeletal muscle.…”

Section: Introductionmentioning

confidence: 99%

See 4 more Smart Citations

Mechanical transients of single toad stomach smooth muscle cells. Effects of lowering temperature and extracellular calcium.

Yamakawa

Harris

Fay

et al. 1990

The Journal of General Physiology

View full text Add to dashboard Cite

Smooth muscle's slow, economical contractions may relate to the kinetics of the crossbridge cycle. We characterized the crossbridge cycle in smooth muscle by studying tension recovery in response to a small, rapid length change (i.e., tension transients) in single smooth muscle cells from the toad stomach (Bufo mar/nus). To confirm that these tension transients reflect crossbridge kinetics, we examined the effect of lowering cell temperature on the tension transient time course. Once this was confirmed, cells were exposed to low extracellular calcium ([Ca~+]o) to determine whether modulation of the cell's shortening velocity by changes in [Ca2+]o reflected the calcium sensitivity of one or more steps in the crossbridge cycle. Single smooth muscle cells were tied between an ultrasensitive force transducer and length displacement device after equilibration in temperature-controlled physiological saline having either a low (0.18 mM) or normal (1.8 mM) calcium concentration. At the peak of isometric force, after electrical stimulation, small, rapid (_<1.8% cell length in 3.6 ms) step stretches and releases were imposed. At room temperature (200C) in normal [Ca~+]o, tension recovery after the length step was described by the sum of two exponentials with rates of 40-90 s -t for the fast phase and 2-4 s -I for the slow phase. In normal [Ca2+]o but at low temperature (10~ the fast tension recovery phase slowed (apparent Oo0 = 1.9) for both stretches and releases whereas the slow tension recovery phase for a release was only moderately affected (apparent 0o0 = 1.4) while unaffected for a stretch. Dynamic stiffness was determined throughout the time course of the tension transient to help correlate the tension transient phases with specific step(s) in the crossbridge cycle. The dissociation of tension and stiffness, during the fast tension recovery phase after a release, was interpreted as evidence that this recovery phase resulted from both the transition of crossbridges from a low-to high-force producing state as well as a transient detachment of crossbridges. From the temperature studies and dynamic stiffness measurements, the slow tension recovery phase most likely reflects the overall rate of crossbridge cycling. From the tension transient studies, it appears that crossbridges cycle slower and have a longer duty cycle in smooth muscle. In low [Ca2+]o at 20~ little effect was observed on the form or time course of the tension transients. These data may indicate that the calcium dependence of the maximum shortening velocity (VmJ (Warshaw, D. M., S. S. Work, and W. J. McBride. 1987b. Pfliigers Archiv. 410:185-191) reflects the calcium sensitivity for one or more steps in the crossbridge cycle that are rate limiting for Vm~ but are not expressed in tension transients. An alternative explanation is the existence of an internal load within the cell that impedes crossbridge cycling as the cell shortens.

show abstract

Section: Extracellular Calcium: Effects On Force Development and Tenssupporting

confidence: 90%

Section: Extracellular Calcium: Effects On Force Development and Tensmentioning

confidence: 66%

Section: Single-cell Preparation and Instrumentationmentioning

confidence: 99%

Section: Extracellular Calcium: Effects On Force Development and Tensmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Mechanical transients of single toad stomach smooth muscle cells. Effects of lowering temperature and extracellular calcium.

Yamakawa

Harris

Fay

et al. 1990

The Journal of General Physiology

View full text Add to dashboard Cite

show abstract

Regulation of force and shortening velocity by calcium and myosin phosphorylation in chemically skinned smooth muscle

Malmqvist

Arner

1996

Pfl�gers Archiv European Journal of Physiology

View full text Add to dashboard Cite

The phosphatase inhibitor okadaic acid (OA) was used to study the relationship between [Ca2+], rates of phosphorylation/dephosphorylation and the mechanical properties of smooth muscle fibres. Force/velocity relationships were determined with the isotonic quick release technique in chemically skinned guinea-pig taenia coli muscles at 22 degrees C. In the maximally thiophosphorylated muscle neither OA (10 microM) nor Ca2+ (increase from pCa 9.0 to pCa 4.5) influenced the force-velocity relationship. When the degree of activation was altered by varying [Ca2+] in the presence of 0.5 microM calmodulin, both force and the maximal shortening velocity (Vmax) were altered. At pCa 5.75, at which force was about 35% of the maximal at pCa 4.5, Vmax was 55% of the maximal value. When OA was introduced into fibres at pCa 6.0, force was increased from less than 5% to 100% of the maximal force obtained in pCa 4.5. The relationship between the degree of myosin light chain phosphorylation and force was similar in the two types of activation; varied [OA] at constant [Ca2+] and at varied [Ca2+]. The relation between force and Vmax when the degree of activation was altered with OA was almost identical to that obtained with varied [Ca2+]. The results show that Ca2+ and OA do not influence force or Vmax in the maximally phosphorylated state and suggest that the level of myosin light chain phosphorylation is the major factor determining Vmax. The finding that the relationship between force and Vmax was similar when activation was altered with OA and Ca2+ suggests, however, that alterations in the absolute rates of phosphorylation and dephosphorylation at a constant phosphorylation level do not influence the mechanical properties of the skinned smooth muscle fibres.

show abstract

Unloaded Shortening Velocity in Single Permeabilized Vascular Smooth Muscle Cells is Independent of Microtubule Status

Zhang

Sherwood

et al. 2004

J Muscle Res Cell Motil

View full text Add to dashboard Cite

Microtubules may influence smooth muscle contraction either via involvement in signal transduction processes or by serving as an internal load that opposes contraction. To test the latter hypothesis, microtubule distribution and the unloaded shortening velocity were investigated in freshly isolated single vascular smooth muscle cells (VSMCs) treated with microtubule modulating drugs. Immunocytochemical studies showed that microtubules run mainly longitudinally in relaxed VSMCs. They are oriented more obliquely, almost transversely to the long axis of the cells after contraction, suggesting that microtubules are compressed during shortening, and thus might impart an internal passive load. Quantitative immunocytochemical analysis revealed that, relative to the control group, colchicine (15 microM) decreased the microtubule density by 40% while taxol (10 microM) increased the microtubule density by 46%. However, alteration of microtubule polymerization status by these microtubule-modulating drugs did not have a significant effect on unloaded shortening velocity in alpha-toxin permeabilized VSMCs under maximal activating conditions or submaximal activating conditions (about 36% of maximal velocity). These results suggest that microtubules do not present an appreciable internal load to dampen single VSMCs shortening in the present experimental system, and that their influence on smooth muscle contraction is primarily via signal transduction mechanisms.

show abstract

Effect of low extracellular calcium on shortening velocity in isolated single smooth muscle cells

Cited by 5 publications

References 24 publications

Mechanical transients of single toad stomach smooth muscle cells. Effects of lowering temperature and extracellular calcium.

Mechanical transients of single toad stomach smooth muscle cells. Effects of lowering temperature and extracellular calcium.

Regulation of force and shortening velocity by calcium and myosin phosphorylation in chemically skinned smooth muscle

Unloaded Shortening Velocity in Single Permeabilized Vascular Smooth Muscle Cells is Independent of Microtubule Status

Contact Info

Product

Resources

About