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Vasomotion dynamics following calcium spiking depend on both cell signalling and limited constriction velocity in rat mesenteric small arteries.

VanBavel E, van der Meulen ET, Spaan JA - J. Cell. Mol. Med. (2008)

Bottom Line: The dirac impulse response of this model had an amplitude that was strongly reduced with increasing perfusion pressure between 17 and 98 mmHg, while time to peak and relaxation time were the largest at an intermediate pressure (57 mmHg: respectively 0.9 and 2.3 sec).In conclusion, this study demonstrates the feasibility of quantitating calcium-activation dynamics in vasomoting small arteries.Performing such analyses during pharmacological intervention and in genetic models provides a tool for unravelling calcium-contraction coupling in small arteries.

View Article: PubMed Central - PubMed

Affiliation: Academic Medical Center, University of Amsterdam, Department of Medical Physics, Amsterdam, The Netherlands. e.vanbavel@amc.uva.nl

ABSTRACT
Vascular smooth muscle cell contraction depends on intracellular calcium. However, calcium-contraction coupling involves a complex array of intracellular processes. Quantitating the dynamical relation between calcium perturbations and resulting changes in tone may help identifying these processes. We hypothesized that in small arteries accurate quantitation can be achieved during rhythmic vasomotion, and questioned whether these dynamics depend on intracellular signalling or physical vasoconstriction. We studied calcium-constriction dynamics in cannulated and pressurized rat mesenteric small arteries ( approximately 300 microm in diameter). Combined application of tetra-ethyl ammonium (TEA) and BayK8644 induced rhythmicity, consisting of regular and irregular calcium spiking and superposition of spikes. Calcium spikes induced delayed vasomotion cycles. Their dynamic relation could be fitted by a linear second-order model. The dirac impulse response of this model had an amplitude that was strongly reduced with increasing perfusion pressure between 17 and 98 mmHg, while time to peak and relaxation time were the largest at an intermediate pressure (57 mmHg: respectively 0.9 and 2.3 sec). To address to what extent these dynamics reside in intracellular signalling or vasoconstriction, we applied rhythmic increases in pressure counteracting the vasoconstriction. This revealed that calcium-activation coupling became faster when vasoconstriction was counteracted. During such compensation, a calcium impulse response remained that lasted 0.5 sec to peak activation, followed by a 1.0 sec relaxation time, attributable to signalling dynamics. In conclusion, this study demonstrates the feasibility of quantitating calcium-activation dynamics in vasomoting small arteries. These dynamics relate to both intracellular signalling and actual vasoconstriction. Performing such analyses during pharmacological intervention and in genetic models provides a tool for unravelling calcium-contraction coupling in small arteries.

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example of superimposed recordings of normalized diameter, calcium and pressure for isobaric loading and seven levels of increasing feedback. Up and down arrows indicate the time of respectively deepest isobaric constriction level and highest pressure during feedback, and the associated signals (mint and black in colour plot). Middle part of the calcium signals has been vertically stretched to better indicate the individual signals. Note that in the presence of feedback, the peak response occurred earlier, while in this particular case the calcium signal decayed actually somewhat slower.
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fig09: example of superimposed recordings of normalized diameter, calcium and pressure for isobaric loading and seven levels of increasing feedback. Up and down arrows indicate the time of respectively deepest isobaric constriction level and highest pressure during feedback, and the associated signals (mint and black in colour plot). Middle part of the calcium signals has been vertically stretched to better indicate the individual signals. Note that in the presence of feedback, the peak response occurred earlier, while in this particular case the calcium signal decayed actually somewhat slower.

Mentions: The dynamics of the calcium effect on diameter may be located in either or both the signalling processes and the smooth muscle cell shortening. If the signalling process were considerably faster than the SMC shortening, then for equal calcium spikes the ‘active pressure’transient under isometric loading would be faster than the isobaric diameter transient. Figure 9 plots an example of superimposed calcium spikes and the associated diameter and pressure transients during various degrees of feedback in a single experiment. Increasing the feedback gain resulted in faster diameter transients. Thus, isobaric peak constriction occurred 1.7 sec after start of the calcium transient, while during the highest gain in this example (k =–9.45 mmHg/% diameter change), peak activation occurred after 1.3 sec.


Vasomotion dynamics following calcium spiking depend on both cell signalling and limited constriction velocity in rat mesenteric small arteries.

VanBavel E, van der Meulen ET, Spaan JA - J. Cell. Mol. Med. (2008)

example of superimposed recordings of normalized diameter, calcium and pressure for isobaric loading and seven levels of increasing feedback. Up and down arrows indicate the time of respectively deepest isobaric constriction level and highest pressure during feedback, and the associated signals (mint and black in colour plot). Middle part of the calcium signals has been vertically stretched to better indicate the individual signals. Note that in the presence of feedback, the peak response occurred earlier, while in this particular case the calcium signal decayed actually somewhat slower.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4401133&req=5

fig09: example of superimposed recordings of normalized diameter, calcium and pressure for isobaric loading and seven levels of increasing feedback. Up and down arrows indicate the time of respectively deepest isobaric constriction level and highest pressure during feedback, and the associated signals (mint and black in colour plot). Middle part of the calcium signals has been vertically stretched to better indicate the individual signals. Note that in the presence of feedback, the peak response occurred earlier, while in this particular case the calcium signal decayed actually somewhat slower.
Mentions: The dynamics of the calcium effect on diameter may be located in either or both the signalling processes and the smooth muscle cell shortening. If the signalling process were considerably faster than the SMC shortening, then for equal calcium spikes the ‘active pressure’transient under isometric loading would be faster than the isobaric diameter transient. Figure 9 plots an example of superimposed calcium spikes and the associated diameter and pressure transients during various degrees of feedback in a single experiment. Increasing the feedback gain resulted in faster diameter transients. Thus, isobaric peak constriction occurred 1.7 sec after start of the calcium transient, while during the highest gain in this example (k =–9.45 mmHg/% diameter change), peak activation occurred after 1.3 sec.

Bottom Line: The dirac impulse response of this model had an amplitude that was strongly reduced with increasing perfusion pressure between 17 and 98 mmHg, while time to peak and relaxation time were the largest at an intermediate pressure (57 mmHg: respectively 0.9 and 2.3 sec).In conclusion, this study demonstrates the feasibility of quantitating calcium-activation dynamics in vasomoting small arteries.Performing such analyses during pharmacological intervention and in genetic models provides a tool for unravelling calcium-contraction coupling in small arteries.

View Article: PubMed Central - PubMed

Affiliation: Academic Medical Center, University of Amsterdam, Department of Medical Physics, Amsterdam, The Netherlands. e.vanbavel@amc.uva.nl

ABSTRACT
Vascular smooth muscle cell contraction depends on intracellular calcium. However, calcium-contraction coupling involves a complex array of intracellular processes. Quantitating the dynamical relation between calcium perturbations and resulting changes in tone may help identifying these processes. We hypothesized that in small arteries accurate quantitation can be achieved during rhythmic vasomotion, and questioned whether these dynamics depend on intracellular signalling or physical vasoconstriction. We studied calcium-constriction dynamics in cannulated and pressurized rat mesenteric small arteries ( approximately 300 microm in diameter). Combined application of tetra-ethyl ammonium (TEA) and BayK8644 induced rhythmicity, consisting of regular and irregular calcium spiking and superposition of spikes. Calcium spikes induced delayed vasomotion cycles. Their dynamic relation could be fitted by a linear second-order model. The dirac impulse response of this model had an amplitude that was strongly reduced with increasing perfusion pressure between 17 and 98 mmHg, while time to peak and relaxation time were the largest at an intermediate pressure (57 mmHg: respectively 0.9 and 2.3 sec). To address to what extent these dynamics reside in intracellular signalling or vasoconstriction, we applied rhythmic increases in pressure counteracting the vasoconstriction. This revealed that calcium-activation coupling became faster when vasoconstriction was counteracted. During such compensation, a calcium impulse response remained that lasted 0.5 sec to peak activation, followed by a 1.0 sec relaxation time, attributable to signalling dynamics. In conclusion, this study demonstrates the feasibility of quantitating calcium-activation dynamics in vasomoting small arteries. These dynamics relate to both intracellular signalling and actual vasoconstriction. Performing such analyses during pharmacological intervention and in genetic models provides a tool for unravelling calcium-contraction coupling in small arteries.

Show MeSH
Related in: MedlinePlus