Rhythmic contractions of isolated small arteries from rat: influence of the endothelium

Gustafsson, Helena; Mulvany, Michael J.; Nilsson, Holger

doi:10.1111/j.1748-1716.1993.tb09545.x

Cited by 81 publications

(86 citation statements)

References 31 publications

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“…Nevertheless, the role of NO and cGMP in the generation of vasomotion is equivocal. Vasomotion was reported to return in endothelium-denuded arteries after incubation with high levels of 8-bromo-cGMP (16); however, others have reported vasomotion or the synchronous Ca 2ϩ signals of vasomotion to be resistant to inhibition of NO synthase (43). Furthermore, NO has been reported to either allow (35) or impede (43) the development of synchronous Ca 2ϩ signals during vasomotion in rat mesenteric arteries.…”

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confidence: 99%

“…An important role is indicated for changes in membrane potential of SMCs and endothelial influences. Indeed, it has been shown that vasomotion in rat mesenteric arteries is accompanied by cyclical changes in membrane potential (12,15,27,29) and is dependent on functional endothelium (16,35). Furthermore, it has been suggested that nitric oxide (NO) from ECs and subsequent elevation of cGMP in SMCs represent the essential contribution of the endothelium to the development of voltage-dependent vasomotion (35).…”

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confidence: 99%

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Essential role of EDHF in the initiation and maintenance of adrenergic vasomotion in rat mesenteric arteries

Mauban

Wier

2004

American Journal of Physiology-Heart and Circulatory Physiology

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confidence: 99%

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confidence: 99%

Essential role of EDHF in the initiation and maintenance of adrenergic vasomotion in rat mesenteric arteries

Mauban

Wier

2004

American Journal of Physiology-Heart and Circulatory Physiology

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“…In the rat iris arteriole, rabbit ear, and superior mesenteric artery, vasomotion is reported to be endothelium independent (3,18,39), whereas in the rat mesenteric, rabbit femoral artery, and hamster aorta, vasomotion is suggested to be endothelium dependent, as shown by its abolition with endothelium denudation (12,21,34,38,40).…”

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confidence: 99%

Endothelial coordination of cerebral vasomotion via myoendothelial gap junctions containing connexins 37 and 40

Haddock

Grayson²,

Brackenbury³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

113

116

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Control of cerebral vasculature differs from that of systemic vessels outside the blood-brain barrier. The hypothesis that the endothelium modulates vasomotion via direct myoendothelial coupling was investigated in a small vessel of the cerebral circulation. In the primary branch of the rat basilar artery, membrane potential, diameter, and calcium dynamics associated with vasomotion were examined using selective inhibitors of endothelial function in intact and endothelium-denuded arteries. Vessel anatomy, protein, and mRNA expression were studied using conventional electron microscopy high-resolution ultrastructural and confocal immunohistochemistry and quantitative PCR. Membrane potential oscillations were present in both endothelial cells and smooth muscle cells (SMCs), and these preceded rhythmical contractions during which adjacent SMC intracellular calcium concentration ([Ca 2ϩ ]i) waves were synchronized. Endothelium removal abolished vasomotion and desynchronized adjacent smooth muscle cell [Ca 2ϩ ]i waves. N G -nitro-L-arginine methyl ester (10 M) did not mimic this effect, and dibutyryl cGMP (300 M) failed to resynchronize [Ca 2ϩ ]i waves in endothelium-denuded arteries. Combined charybdotoxin and apamin abolished vasomotion and depolarized and constricted vessels, even in absence of endothelium. Separately, 37,43 Gap27 and 40 Gap27 abolished vasomotion. Extensive myoendothelial gap junctions (3 per endothelial cell) composed of connexins 37 and 40 connected the endothelial cell and SMC layers. Synchronized vasomotion in rat basilar artery is endothelium dependent, with [Ca 2ϩ ]i waves generated within SMCs being coordinated by electrical coupling via myoendothelial gap junctions.connexin; electron microscopy; endothelial function; potassium channel; membrane potential VASOMOTION is an intrinsic feature of many arteries and arterioles under normal and pathological conditions and may contribute to regulation of blood flow and pressure (1,14). Both spontaneous and agonist-induced vasomotion occur when oscillations in the concentration of intracellular calcium ([Ca 2ϩ ] i ) become synchronized among adjacent smooth muscle cells, giving rise to global oscillations in [Ca 2ϩ ] i across the vessel wall (13,15,26,27,33,41,(47)(48)(49).There is clear heterogeneity in the mechanisms that underlie vasomotion, and specifically whether the endothelium plays a mandatory or modulatory role. In the rat iris arteriole, rabbit ear, and superior mesenteric artery, vasomotion is reported to be endothelium independent (3, 18, 39), whereas in the rat mesenteric, rabbit femoral artery, and hamster aorta, vasomotion is suggested to be endothelium dependent, as shown by its abolition with endothelium denudation (12,21,34,38,40).Endothelium-dependent effects on vasomotion have been attributed to the vasodilatory factors nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF). In some studies, endothelial cells play an essential role in synchronizing the activity of smooth muscle cells through the rel...

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“…In the vascular wall, synchronized oscillations of smooth muscle cell tension give rise to oscillations of vascular tone (vasomotion), which are of physiological and pathophysiological importance. 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.…”

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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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Rhythmic contractions of isolated small arteries from rat: influence of the endothelium

Cited by 81 publications

References 31 publications

Essential role of EDHF in the initiation and maintenance of adrenergic vasomotion in rat mesenteric arteries

Essential role of EDHF in the initiation and maintenance of adrenergic vasomotion in rat mesenteric arteries

Endothelial coordination of cerebral vasomotion via myoendothelial gap junctions containing connexins 37 and 40

Hypothesis for the Initiation of Vasomotion

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