Interactions between membrane potential and intracellular calcium concentration in vascular smooth muscle

Nilsson, Mats

doi:10.1046/j.1365-201x.1998.00435.x

Cited by 21 publications

(16 citation statements)

References 66 publications

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“…One is the question of the nature of the ion channel. Ca 2ϩ -activated inward currents have been demonstrated in vascular smooth muscle to be either cation or chloride currents [25][26][27][28][29] ; to our knowledge, none of these has been characterized as being cGMP dependent. There are other questions regarding the action of cGMP: Does cGMP act directly on the channels, is this action mediated via protein kinase G on the channel, or does the action of cGMP possibly influence the magnitude or direction of Ca 2ϩ release instead?…”

Section: Discussionmentioning

confidence: 99%

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: Discussionmentioning

confidence: 99%

Hypothesis for the Initiation of Vasomotion

Peng

Matchkov

Ivarsen

et al. 2001

Circulation Research

232

351

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“…This concentration gradient is particularly important for contraction and relaxation of vascular smooth muscle (VSM) cells [4][5][6][7]. Among the mechanisms utilized by VSM and other cells to maintain this concentration gradient, calcium channels located on the cell membrane play a key role.…”

Section: Location Structure and Function Of Calcium Channelsmentioning

confidence: 99%

Calcium channel blockers: pharmacology and place in therapy of pediatric hypertension

Flynn

Pasko

2000

Pediatric Nephrology

105

104

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The calcium channel blockers (CCBs) are a diverse group of antihypertensive medications with variable pharmacokinetics and clinical effects. Although CCBs have been widely applied to the treatment of hypertensive children, data regarding the pharmacokinetics, efficacy and safety of these agents in children are extremely limited. In this review we briefly summarize the mechanism of action of CCBs and then summarize pertinent pharmacokinetic information on each of the CCBs commonly used in children, including amlodipine, diltiazem, felodipine, isradipine, intravenous nicardipine, nifedipine and verapamil. Clinically important drug interactions and adverse effects are discussed, as well as the potential role of CCBs in renal protection. Available pediatric efficacy and safety data are summarized, and recommendations made regarding the rational use of CCBs in the management of pediatric hypertension.

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“…A rise in intracellular free [Ca 2ϩ ] and sensitization of the contractile machinery to Ca 2ϩ are key features in receptor-mediated agonist activation of smooth muscle (27). Clear evidence has been presented that the sustained phase of responses to norepinephrine and carbachol is influenced by sensitization (18,23,28).…”

Section: Discussionmentioning

confidence: 99%

“…Norepinephrine-induced activation involves Ca 2ϩ release from the sarcoplasmic reticulum (30). The role of the released Ca 2ϩ is dual: to activate the contractile machinery directly and to regulate Ca 2ϩ -sensitive channel activity, which alters the membrane potential and Ca 2ϩ channel influx (16,27,31). The sarcoplasmic reticulum in phasic muscle, such as the portal vein, is poorly developed (7).…”

Section: Discussionmentioning

confidence: 99%

Sustained norepinephrine contraction in the rat portal vein is lost when Ca²⁺ is replaced with Sr²⁺

Bonnevier

Malmqvist

Sonntag

et al. 2002

American Journal of Physiology-Cell Physiology

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Agonist-induced activation of smooth muscle involves a rise in intracellular Ca2+ concentration and sensitization of myosin light chain phosphorylation to Ca2+. Sr2+ can enter through Ca2+channels, be sequestered and released from sarcoplasmic reticulum, and replace Ca2+ in activation of myosin light chain phosphorylation. Sr2+ cannot replace Ca2+ in facilitation of agonist-activated Ca2+-dependent nonselective cation channels. It is not known whether Sr2+can replace Ca2+ in small G protein-mediated sensitization of phosphorylation. To explore mechanisms involved in α-receptor-activated contractions in smooth muscle, effects of replacing Ca2+ with Sr2+ were examined in rat portal vein. Norepinephrine (NE) at >3.0 × 10−7 M in the presence of Ca2+ resulted in a strong sustained contraction, whereas this sustained component was absent in the presence of Sr2+; only the amplitude of phasic contractions increased. Pretreatment with low (∼0.05 mM) free Ca2+followed by 2.5 mM Sr2+ resulted in a sustained component of the NE response. In β-escin-permeabilized preparations, phenylephrine in the presence of GTP or guanosine 5′- O-(3-thiotriphosphate) alone induced sensitization to Sr2+. In conclusion, a Ca2+-regulated membrane/channel process is required for the sustained component of NE responses in rat portal vein. Sensitization alone is not responsible for the sustained phase of the NE contraction.

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Interactions between membrane potential and intracellular calcium concentration in vascular smooth muscle

Cited by 21 publications

References 66 publications

Hypothesis for the Initiation of Vasomotion

Hypothesis for the Initiation of Vasomotion

Calcium channel blockers: pharmacology and place in therapy of pediatric hypertension

Sustained norepinephrine contraction in the rat portal vein is lost when Ca²⁺ is replaced with Sr²⁺

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Interactions between membrane potential and intracellular calcium concentration in vascular smooth muscle

Cited by 21 publications

References 66 publications

Hypothesis for the Initiation of Vasomotion

Hypothesis for the Initiation of Vasomotion

Calcium channel blockers: pharmacology and place in therapy of pediatric hypertension

Sustained norepinephrine contraction in the rat portal vein is lost when Ca2+ is replaced with Sr2+

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Sustained norepinephrine contraction in the rat portal vein is lost when Ca²⁺ is replaced with Sr²⁺