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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 vasomotion and calcium oscillations during periods of proportional feedback counteracting the constriction by simultaneously raising the pressure. In this particular case, vasomotion was regular. Three periods of increasing feedback gain are shown, leading to smaller diameter excursions and larger pressure oscillations. The calcium signal was not affected by such periods of non-isobaric loading.
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fig07: Example of vasomotion and calcium oscillations during periods of proportional feedback counteracting the constriction by simultaneously raising the pressure. In this particular case, vasomotion was regular. Three periods of increasing feedback gain are shown, leading to smaller diameter excursions and larger pressure oscillations. The calcium signal was not affected by such periods of non-isobaric loading.

Mentions: Figure 7 depicts an example of vasomotion during non-isobaric loading. The feedback system was activated for only a few cycles, in order to prevent possible alterations in the level of vasoconstriction. Feedback was always started when the vasomoting vessel was at its maximal diameter. This way, constrictions are exchanged for transient increases in pressure. In this example, three periods of proportional feedback application at increasing gain are shown. As expected, a larger feedback gain resulted in a smaller diameter amplitude and a larger pressure amplitude. Non-isobaric loading for the indicated short periods did not affect the calcium spikes.


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 vasomotion and calcium oscillations during periods of proportional feedback counteracting the constriction by simultaneously raising the pressure. In this particular case, vasomotion was regular. Three periods of increasing feedback gain are shown, leading to smaller diameter excursions and larger pressure oscillations. The calcium signal was not affected by such periods of non-isobaric loading.
© Copyright Policy
Related In: Results  -  Collection

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

fig07: Example of vasomotion and calcium oscillations during periods of proportional feedback counteracting the constriction by simultaneously raising the pressure. In this particular case, vasomotion was regular. Three periods of increasing feedback gain are shown, leading to smaller diameter excursions and larger pressure oscillations. The calcium signal was not affected by such periods of non-isobaric loading.
Mentions: Figure 7 depicts an example of vasomotion during non-isobaric loading. The feedback system was activated for only a few cycles, in order to prevent possible alterations in the level of vasoconstriction. Feedback was always started when the vasomoting vessel was at its maximal diameter. This way, constrictions are exchanged for transient increases in pressure. In this example, three periods of proportional feedback application at increasing gain are shown. As expected, a larger feedback gain resulted in a smaller diameter amplitude and a larger pressure amplitude. Non-isobaric loading for the indicated short periods did not affect the calcium spikes.

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