Membrane hyperpolarization inhibits agonist‐induced synthesis of inositol 1,4,5‐trisphosphate in rabbit mesenteric artery.

Itoh, Takeo; Seki, Nobuhiko; Suzuki, Satoshi; S, Itó; Kajikuri, Junko; Kuriyama, Hirosi

doi:10.1113/jphysiol.1992.sp019166

Cited by 187 publications

(169 citation statements)

References 30 publications

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“…We show here that voltage-dependent activation of G o protein through VGSCs resulted in IP 3 formation and intracellular Ca 2ϩ release. Evidence for depolarization-induced IP 3 formation has been previously reported in skeletal muscle (25), and hyperpolarization has been suggested to reduce agonist-induced generation of IP 3 in rabbit mesenteric artery (26). Thus, the voltage-dependent activation of G o protein and IP 3 synthesis observed here may not be specific for cerebellar granule cells.…”

Section: Discussionmentioning

confidence: 47%

Permissive Effect of Voltage on mGlu 7 Receptor Subtype Signaling in Neurons

Perroy

Richard

Nargeot

et al. 2002

Journal of Biological Chemistry

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G protein-coupled receptors mobilize neuronal signaling cascades which until now have not been shown to depend on the state of membrane depolarization. Thus we have previously shown that the metabotropic glutamate receptor type 7 (mGlu7 receptor) blocks P/Q-type Ca 2؉ channels via activation of a G o protein and PKC, in cerebellar granule cells. We show here that the transient depolarizations used to evoke the studied Ca 2؉ current were indeed permissive to activate this pathway by a mGlu7 receptor agonist. Indeed, sustained depolarization to 0 mV was sufficient to inhibit P/Q-type Ca 2؉ channels. This effect involved a conformational change in voltage-gated sodium channel independently of Na ؉ flux, activation of a pertussis toxin-sensitive G-protein, inositol trisphosphate formation, intracellular Ca 2؉ release, and PKC activity. Subliminal sustained membrane depolarization became efficient in inducing inositol trisphosphate formation, release of intracellular Ca 2؉ and in blocking Ca 2؉ channels, when applied concomitantly with the mGlu7a receptor agonist, D,L-aminophosphonobutyrate. This synergistic effect of membrane depolarization and mGlu7 receptor activation provides a mechanism by which neuronal excitation could control action of the mGlu7 receptor in neurons.The excitatory neurotransmitter, glutamate, mediates its effects by activating ionotropic and metabotropic (mGlu) receptors. Eight genes encoding mGlu receptors have been identified and classified into three groups. The group I (mGlu1 and mGlu5 receptors) activates PLC through a G q protein, whereas group II (mGlu2 and mGlu3 receptors) and group III (mGlu4, mGlu6, mGlu7, and mGlu8 receptors) are coupled to G i /G o proteins (1). These receptors are widely distributed throughout the mammalian brain (2-5), but only the mGlu7 receptor subtype is almost exclusively localized at presynaptic sites (6 -8).Group II and III mGlu receptors, and particularly the mGlu7 receptor subtype, inhibit synaptic transmission (1, 9). Thus in vitro studies have shown that stimulation of mGlu7 receptors decreases release of glutamate in cerebellar cultures (10) and GABA in striatal cultures (11), promoting neuroprotection and excitotoxicity, respectively. Moreover, we have recently shown that mGlu7 receptors selectively block P/Q-type Ca 2ϩ channels in neurons (12), and these channels control transmitter release (13). Together these studies suggest that mGlu7 receptors play an important role in the modulation of synaptic transmission.Recent studies have pointed out that in the rat locus coeruleus, group III mGlu receptor agonists down-regulate high but not low frequency synaptic activity (14), suggesting that this receptor action depends on the state of neuronal depolarization. Moreover, a voltage-dependent activation of a G o protein has recently been shown in rat brain synaptoneurosomes (15). In light of these results, and because the mGlu7 receptor is coupled to a G o protein, this receptor is a potential candidate for mobilization of both voltage-and G o protein-depen...

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Section: Discussionmentioning

confidence: 47%

Permissive Effect of Voltage on mGlu 7 Receptor Subtype Signaling in Neurons

Perroy

Richard

Nargeot

et al. 2002

Journal of Biological Chemistry

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“…It had been reported in several cell types (including arterial myocytes) that agonist-induced Ca 2ϩ release from internal stores can be modulated by the cell's membrane potential. However, this phenomenon was not associated with L-type Ca 2ϩ channel activation but was attributed to the existence of a voltage-dependent step in the PLC-activation͞InsP 3 synthesis pathway (8)(9)(10). Here, we report that CCICR is, indeed, selectively regulated by low concentrations of extracellular ATP, an agent coreleased with norepinephrine (NE) from sympathetic terminals and from cells (erythrocytes and platelets) damaged during vascular injury (11)(12)(13).…”

mentioning

confidence: 85%

“…These findings are in excellent agreement with the data obtained in single myocytes, demonstrating that CCICR (the coupling of Ca 2ϩ channels to the SR through the activation of the PLC͞InsP 3 pathway) can be triggered by either membrane depolarization or FPL. The CCICR helps to explain the dependence of InsP 3 -dependent Ca 2ϩ release on the membrane potential observed in smooth muscle (8,9) and other cell types (7,10); however, the possibility that there is a voltage-dependent step at the level of either G protein or PLC activation (8-10) cannot be fully excluded.…”

Section: Discussionmentioning

confidence: 99%

Metabotropic Ca ²⁺ channel-induced Ca ²⁺ release and ATP-dependent facilitation of arterial myocyte contraction

Valle‐Rodríguez

Calderón

Ruiz

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

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Voltage-gated Ca 2؉ channels in arterial myocytes can mediate Ca 2؉ release from the sarcoplasmic reticulum and, thus, induce contraction without the need of extracellular Ca 2؉ influx. This metabotropic action of Ca 2؉ channels (denoted as calcium-channelinduced calcium release or CCICR) involves activation of G proteins and the phospholipase C-inositol 1,4,5-trisphosphate pathway. Here, we show a form of vascular tone regulation by extracellular ATP that depends on the modulation of CCICR. In isolated arterial myocytes, ATP produced facilitation of Ca 2؉ -channel activation and, subsequently, a strong potentiation of CCICR. The facilitation of L-type channel still occurred after full blockade of purinergic receptors and inhibition of G proteins with GDP␤S, thus suggesting that ATP directly interacts with Ca 2؉ channels. The effects of ATP appear to be highly selective, because they were not mimicked by other nucleotides (ADP or UTP) or vasoactive agents, such as norepinephrine, acetylcholine, or endothelin-1. We have also shown that CCICR can trigger arterial cerebral vasoconstriction in the absence of extracellular calcium and that this phenomenon is greatly facilitated by extracellular ATP. Although, at low concentrations, ATP does not induce arterial contraction per se, this agent markedly potentiates contractility of partially depolarized or primed arteries. Hence, the metabotropic action of L-type Ca 2؉ channels could have a high impact on vascular pathophysiology, because, even in the absence of Ca 2؉ channel opening, it might mediate elevations of cytosolic Ca 2؉ and contraction in partially depolarized vascular smooth muscle cells exposed to small concentrations of agonists.L-type Ca 2ϩ channel ͉ vascular contractility ͉ excitation-contraction coupling C ontraction of vascular smooth muscle cells (VSMCs) determines vessel diameter and, thus, regulates blood flow and pressure. VSMC contraction is triggered by a rise of cytosolic calcium ion concentration ([Ca 2ϩ ]) due to either transmembrane Ca 2ϩ influx or Ca 2ϩ release from the sarcoplasmic reticulum (SR). Extracellular Ca 2ϩ entry normally occurs through L-type voltagedependent Ca 2ϩ channels, although there are numerous ligandgated membrane channels that are also Ca 2ϩ permeable (1). Ca 2ϩ release from the SR is mediated by inositol trisphosphate (InsP 3 ) and ryanodine receptors. Vasoactive agents acting on the different vascular territories induce VSMC contraction by binding to membrane receptors and the subsequent activation of one or more of the Ca 2ϩ -entry and͞or Ca 2ϩ -release channels (2-5).We have described a previously unnoticed metabotropic effect of vascular L-type Ca 2ϩ channels, denoted as calcium-channelinduced Ca 2ϩ release (CCICR), which requires Ca 2ϩ channel activation but is independent of extracellular Ca 2ϩ influx (6). This new Ca 2ϩ -release mechanism depends on the conformational change of L-type Ca 2ϩ channels and the downstream activation of the G protein͞phospholipase C (PLC) cascade, leading to synthesis of InsP 3 and C...

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“…Although GPCR activation is not normally considered to be directly sensitive to changes in the cell membrane potential, studies in a variety of cell types now support this concept (3)(4)(5)(6)(7). In particular, Ca 2ϩ release stimulated by P2Y receptors in rat megakaryocytes or muscarinic cholinergic receptors in coronary artery smooth muscle is potentiated by depolarization and inhibited by hyperpolarization (5,7,8).…”

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confidence: 90%

Direct Voltage Control of Signaling via P2Y1 and Other Gαq-coupled Receptors

Martı́nez-Pinna

Gurung

Vial

et al. 2005

Journal of Biological Chemistry

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Membrane hyperpolarization inhibits agonist‐induced synthesis of inositol 1,4,5‐trisphosphate in rabbit mesenteric artery.

Cited by 187 publications

References 30 publications

Permissive Effect of Voltage on mGlu 7 Receptor Subtype Signaling in Neurons

Permissive Effect of Voltage on mGlu 7 Receptor Subtype Signaling in Neurons

Metabotropic Ca ²⁺ channel-induced Ca ²⁺ release and ATP-dependent facilitation of arterial myocyte contraction

Direct Voltage Control of Signaling via P2Y1 and Other Gαq-coupled Receptors

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Membrane hyperpolarization inhibits agonist‐induced synthesis of inositol 1,4,5‐trisphosphate in rabbit mesenteric artery.

Cited by 187 publications

References 30 publications

Permissive Effect of Voltage on mGlu 7 Receptor Subtype Signaling in Neurons

Permissive Effect of Voltage on mGlu 7 Receptor Subtype Signaling in Neurons

Metabotropic Ca 2+ channel-induced Ca 2+ release and ATP-dependent facilitation of arterial myocyte contraction

Direct Voltage Control of Signaling via P2Y1 and Other Gαq-coupled Receptors

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Metabotropic Ca ²⁺ channel-induced Ca ²⁺ release and ATP-dependent facilitation of arterial myocyte contraction