Rhythmic contractions of isolated small arteries from rat: role of calcium

Gustafsson, Helena; Nilsson, Holger

doi:10.1111/j.1748-1716.1993.tb09623.x

Cited by 55 publications

(44 citation statements)

References 22 publications

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“…This has been demonstrated previously 5,6 and is confirmed in the present study. Also, the oscillations of [Ca 2ϩ ] i and tension were always prevented by inhibitors of the SR function (Table).…”

Section: Resultssupporting

confidence: 81%

“…1,2 Vasomotion is known to be associated with slow oscillations of smooth muscle membrane potential 3 and of intracellular Ca 2ϩ concentration ([Ca 2ϩ ] i ). 4 It has also been demonstrated that the function of the sarcoplasmic reticulum (SR) is critically important for the activity, 5,6 whereas potassium channels play only a modulatory role. 7,8 The role of the endothelium differs between vascular beds.…”

mentioning

confidence: 99%

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Hypothesis for the Initiation of Vasomotion

Peng

Matchkov

Ivarsen

et al. 2001

Circulation Research

232

351

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Abstract-Vasomotion is the regular variation in tone of arteries. In our study, we suggest a model for the initiation of vasomotion. We suggest that intermittent release of Ca 2ϩ from the sarcoplasmic reticulum (SR, cytosolic oscillator), which is initially unsynchronized between the vascular smooth muscle cells, becomes synchronized to initiate vasomotion. The synchronization is achieved by an ion current over the cell membrane, which is activated by the oscillating Ca 2ϩ release. This current results in an oscillating membrane potential, which synchronizes the SR in the vessel wall and starts vasomotion. Therefore, the pacemaker of the vascular wall can be envisaged as a diffuse array of individual cytosolic oscillators that become entrained by a reciprocal interaction with the cell membrane. The model is supported by experimental data. Confocal [Ca 2ϩ ] i imaging and isometric force development in isolated rat resistance arteries showed that low norepinephrine concentrations induced SR-dependent unsynchronized waves of Ca 2ϩ in the vascular smooth muscle. In the presence of the endothelium, the waves converted to global synchronized oscillations of [Ca 2ϩ ] i after some time, and vasomotion appeared. Synchronization was also seen in the absence of endothelium if 8-bromo-cGMP was added to the bath. Using the patch-clamp technique and microelectrodes, we showed that Ca 2ϩ release can activate an inward current in isolated smooth muscle cells from the arteries and cause depolarization. These electrophysiological effects of Ca 2ϩ release were cGMP dependent, which is consistent with the possibility that they are important for the cGMP-dependent synchronization. Further support for the model is the observation that a short-lasting current pulse can initiate vasomotion in an unsynchronized artery as expected from the model.

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Section: Resultssupporting

confidence: 81%

mentioning

confidence: 99%

Hypothesis for the Initiation of Vasomotion

Peng

Matchkov

Ivarsen

et al. 2001

Circulation Research

232

351

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“…Some previous models of vasomotion have assumed that oscillations are intrinsic to the intracellular dynamics of smooth muscle activation (Achakri et al, 1994;Gonzalez-Fernandez & Ermentrout, 1994;Parthimos et al, 1999Parthimos et al, , 2007Peng et al, 2001;Gustafsson & Nilsson, 1993b). In the present model, the dynamics of activation are governed by a simple first-order differential equation that has no intrinsic oscillatory behaviour.…”

Section: Discussionmentioning

confidence: 90%

Spontaneous oscillations in a model for active control of microvessel diameters

Arciero

Secomb²

2011

Mathematical Medicine and Biology

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A new theory is presented for the origin of spontaneous oscillations in blood vessel diameters that are observed experimentally in the microcirculation. These oscillations, known as vasomotion, involve timevarying contractions of the vascular smooth muscle in the walls of arterioles. It is shown that such oscillations can arise as a result of interactions between the mechanics of the vessel wall and the dynamics of the active contraction of smooth muscle cells in response to circumferential tension in the wall. A theoretical model is developed in which the diameter and the degree of activation in a vessel are dynamic variables. The model includes effects of wall shear stress and oxygen-dependent metabolic signals on smooth muscle activation and is applied to a single vessel and to simplified network structures. The model equations predict limit cycle oscillations for certain ranges of parameters such as wall shear stress, arterial pressure and oxygen consumption rate. Predicted characteristics of the oscillations, including their sensitivity to arterial pressure, are consistent with experimental observations.

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“…Studies on RC have been undertaken for more than 150 years [10][11][12][13] , after the first report by Jones regarding the veins of bats' wings in 1852 [11] . To date, the mechanism of RC is still not very clear, and plenty of cellular components of the vascular smooth muscle cell have been reported to participate in generating RC; these include RyR and the Ca 2+ -pump of SR, the L-type Ca 2+ channel, the K + channel, Na + , K + -ATPase and the nitric oxide (NO)-cGMP system.…”

Section: Introductionmentioning

confidence: 99%

Doxorubicin-induced vasomotion and [Ca2+]i elevation in vascular smooth muscle cells from C57BL/6 mice

Shen

Chun-ling

et al. 2009

Acta Pharmacol Sin

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Aim: To explore the action of doxorubicin on vascular smooth muscle cells. Methods: Isometric tension of denuded or intact thoracic aortic vessels was recorded and [Ca 2+ ] i in isolated aortic smooth muscle cells was measured by using Fluo-3. Results: Doxorubicin induced phasic and tonic contractions in denuded vessels and increased levels of [Ca 2+ ] i in single muscle cells. Treatment with 10 µmol/L ryanodine had no effect on basal tension, but it did abolish doxorubicin-induced phasic contraction. Treatment with 10 mmol/L caffeine induced a transient phasic contraction only, and the effect was not significantly altered by ryanodine, the omission of extracellular Ca 2+ or both. Phenylephrine induced rhythmic contraction (RC) in intact vessels. Treatment with 100 µmol/L doxorubicin enhanced RC amplitude, but 1 mmol/L doxorubicin abolished RC, with an increase in maximal tension. Caffeine at 100 µmol/L increased the frequency of the RC only. In the presence of 100 µmol/L caffeine, however, 100 µmol/L doxorubicin abolished the RC and decreased its maximal tension. Treatment with 10 µmol/L ryanodine abolished the RC, with an increase in the maximal tension. In Ca 2+ -free solution, doxorubicin induced a transient [Ca 2+ ] i increase that could be abolished by ryanodine pretreatment in single muscle cells. The doxorubicin-induced increase in [Ca 2+ ] i was suppressed by nifedipine and potentiated by ryanodine and charybdotoxin. Conclusion: Doxorubicin not only releases Ca 2+ from the sarcoplasmic reticulum but also promotes the entry of extracellular Ca 2+ into vascular smooth muscle cells.

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Rhythmic contractions of isolated small arteries from rat: role of calcium

Cited by 55 publications

References 22 publications

Hypothesis for the Initiation of Vasomotion

Hypothesis for the Initiation of Vasomotion

Spontaneous oscillations in a model for active control of microvessel diameters

Doxorubicin-induced vasomotion and [Ca2+]i elevation in vascular smooth muscle cells from C57BL/6 mice

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