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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 predicting the diameter response to a hypothetical dirac pulse in the calcium signal for a single vessel at the three studied levels of pressure, using the second-order model. The shape of these curves was characterized by three pragmatic parameters: the time to peak, amplitude and half-maximal diameter relaxation time, shown here for the response at 17 mmHg.
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fig05: Example of predicting the diameter response to a hypothetical dirac pulse in the calcium signal for a single vessel at the three studied levels of pressure, using the second-order model. The shape of these curves was characterized by three pragmatic parameters: the time to peak, amplitude and half-maximal diameter relaxation time, shown here for the response at 17 mmHg.

Mentions: The above fitting procedures were performed on 486 periods of vasomotion in nine vessels at three pressures, resulting in 486 sets of parameters for each model. Subsequently, averages of the parameters were determined for each vessel and each pressure. In addition, the parameters obtained for model II were used to calculate the diameter response to a Dirac calcium impulse (i.e. an impulse with infinite amplitude, zero duration, and unity area under the curve), since this best characterizes the behaviour of the system in the time domain. Three descriptive parameters were then deduced from the impulse response (see also Fig. 5): the peak impulse response, the time of peak response, and the time of half-maximal relaxation. These descriptive parameters were also averaged for each vessel and pressure level.


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 predicting the diameter response to a hypothetical dirac pulse in the calcium signal for a single vessel at the three studied levels of pressure, using the second-order model. The shape of these curves was characterized by three pragmatic parameters: the time to peak, amplitude and half-maximal diameter relaxation time, shown here for the response at 17 mmHg.
© Copyright Policy
Related In: Results  -  Collection

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

fig05: Example of predicting the diameter response to a hypothetical dirac pulse in the calcium signal for a single vessel at the three studied levels of pressure, using the second-order model. The shape of these curves was characterized by three pragmatic parameters: the time to peak, amplitude and half-maximal diameter relaxation time, shown here for the response at 17 mmHg.
Mentions: The above fitting procedures were performed on 486 periods of vasomotion in nine vessels at three pressures, resulting in 486 sets of parameters for each model. Subsequently, averages of the parameters were determined for each vessel and each pressure. In addition, the parameters obtained for model II were used to calculate the diameter response to a Dirac calcium impulse (i.e. an impulse with infinite amplitude, zero duration, and unity area under the curve), since this best characterizes the behaviour of the system in the time domain. Three descriptive parameters were then deduced from the impulse response (see also Fig. 5): the peak impulse response, the time of peak response, and the time of half-maximal relaxation. These descriptive parameters were also averaged for each vessel and pressure level.

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