Inositol 1,4,5-trisphosphate-induced Ca2+ release is regulated by cytosolic Ca2+ in intact skeletal muscle

López, José R.; Terzic, André

doi:10.1007/s004240050199

Cited by 10 publications

(4 citation statements)

References 42 publications

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“…Furthermore, since InsP 3 and ryanodine applied together failed to increase the Ca 2+ sensitivity of myofilaments [34], the InsP 3 -induced contractile response could not be related to an effect on the contractile apparatus. Thus, these data are in agreement with those previously obtained in a study on skeletal muscle [20]. Furthermore, after the application of InsP 3 , the residual tension induced by cooling in the presence of ryanodine disappeared.…”

Section: The Effect Of Insp 3 On Rccs After Ryanodine Treatmentsupporting

confidence: 94%

Rapid cooling-induced contractures in rat skinned skeletal muscle fibres originate from sarcoplasmic reticulum Ca2+ release through ryanodine and inositol trisphosphate receptors

Talon¹,

Huchet-Cadiou²,

Léoty³

2000

Pflügers Arch - Eur J Physiol

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Previous reports have shown that cooling striated muscles induces contractile responses that are related to Ca2+ release from the sarcoplasmic reticulum. However, the effect of cooling has generally been studied in the presence of pharmacological agents that potentiate rapid cooling-induced contractures. The present study shows that in saponin-skinned rat skeletal muscle preparations, a drop in temperature from 22 degrees C to 2 degrees C per se induces a contracture which relaxes on return to 22 degrees C. In fast-twitch fibres, rapid cooling-induced contractures are fully blocked by ryanodine, an inhibitor of ryanodine receptors. By contrast, in slow-twitch fibres, ryanodine partially inhibits the rapid cooling-induced contractile response, leaving a residual tension that dissipates after application of inositol 1,4,5-trisphosphate (InsP3). At low concentrations, heparin, an inhibitor of InsP3 receptors, decreases rapid cooling-induced contractures in both types of muscle. The present results suggest that in skeletal muscle, rapid cooling-induced contractures are due to both ryanodine-sensitive and InsP3-sensitive Ca2+ release from the sarcoplasmic reticulum.

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Section: The Effect Of Insp 3 On Rccs After Ryanodine Treatmentsupporting

confidence: 94%

Rapid cooling-induced contractures in rat skinned skeletal muscle fibres originate from sarcoplasmic reticulum Ca2+ release through ryanodine and inositol trisphosphate receptors

Talon¹,

Huchet-Cadiou²,

Léoty³

2000

Pflügers Arch - Eur J Physiol

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“…In cardiomyocytes isolated from Chagas' patients [IP 3 ] i was higher compared to those from control subjects. It has been previously shown in various types of cells that elevation of IP 3 production, which release Ca 2+ from intracellular stores [24,69] [69] and a robust Ca 2+ release upon exposure to IP 3 BM-, ET-1-, or BK [69]. The elevated intracellular [IP 3 ] can have two possible sources i) the plasma membrane of parasites in intracellular forms, such as amastigotes [70] and ii) IP 3 derived from the plasma membrane of the host changes due to changes in IP 3 synthesis and/or degradation [71,72].…”

Section: Plos Neglected Tropical Diseasesmentioning

confidence: 99%

Increases in [IP3]i aggravates diastolic [Ca2+] and contractile dysfunction in Chagas’ human cardiomyocytes

Mijares

Espinosa²,

Adams

et al. 2020

PLoS Negl Trop Dis

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Chagas cardiomyopathy is the most severe manifestation of human Chagas disease and represents the major cause of morbidity and mortality in Latin America. We previously demonstrated diastolic Ca 2+ alterations in cardiomyocytes isolated from Chagas' patients to different degrees of cardiac dysfunction. In addition, we have found a significant elevation of diastolic [Na + ] d in Chagas' cardiomyocytes (FCII>FCI) that was greater than control. Exposure of cardiomyocytes to agents that enhance inositol 1,4,5 trisphosphate (IP 3) generation or concentration like endothelin (ET-1) or bradykinin (BK), or membrane-permeant myoinositol 1,4,5-trisphosphate hexakis(butyryloxy-methyl) esters (IP 3 BM) caused an elevation in diastolic [Ca 2+ ] ([Ca 2+ ] d) that was always greater in cardiomyocytes from Chagas' than non-Chagas' subjects, and the magnitude of the [Ca 2+ ] d elevation in Chagas' cardiomyocytes was related to the degree of cardiac dysfunction. Incubation with xestospongin-C (Xest-C), a membrane-permeable selective blocker of the IP 3 receptors (IP 3 Rs), significantly reduced [Ca 2+ ] d in Chagas' cardiomyocytes but did not have a significant effect on non-Chagas' cells. The effects of ET-1, BK, and IP 3 BM on [Ca 2+ ] d were not modified by the removal of extracellular [Ca 2+ ] e. Furthermore, cardiomyocytes from Chagas' patients had a significant decrease in the sarcoplasmic reticulum (SR) Ca 2+ content compared to control (Control>F-CI>FCII), a higher intracellular IP 3 concentration ([IP 3 ] i) and markedly depressed contractile properties compared to control cardiomyocytes. These results provide additional and convincing support about the implications of IP 3 in the pathogenesis of Chagas cardiomyopathy in patients at different stages of chronic infection. Additionally, these findings open the door for novel therapeutic strategies oriented to improve cardiac function and quality of life of individuals suffering from chronic Chagas cardiomyopathy (CC).

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“…5). Heparin, which inhibits IP× receptor activation (Vaca & Kunze, 1995;Lopez & Terzic, 1996), reduced the effect of metabotropic agonists. Heparin reduced the effect of trans-ACPD by 72% (from 15·8 ± 1·8 to 4·4 ± 1 % reduction of barium current), of l-CCG_I by 70% (from 14·5 ± 1·8 to 4·3 ± 0·9 %) and of l_AP4 by 69% (from 10·1 ± 1·9 to 3·1 ± 0·7 %).…”

Section: Metabotropic Glutamate Receptor Pharmacologymentioning

confidence: 99%

Metabotropic and ionotropic glutamate receptors regulate calcium channel currents in salamander retinal ganglion cells

Shen

Slaughter

1998

The Journal of Physiology

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We chose to examine the glutamatergic regulation of calcium currents in amphibian retinal ganglion cells. These neurons possess a plethora of glutamate receptors, including the AMPAÏkainate and NMDA ionotropic receptors (Slaughter & Miller, 1983) and at least one form of metabotropic receptor (Akopian & Witkovsky, 1996). Additionally, these neurons are thought to be purely postsynaptic in the retina and therefore ionotropic and metabotropic receptors may function in a unique manner to control postsynaptic integration rather than regulation of transmitter release. Recordings from ganglion cells revealed sustained, highvoltage-activated calcium channel currents. These currents were suppressed by both ionotropic and metabotropic glutamate agonists. Ganglion cells possessed all three groups of metabotropic receptor, although group III agonists produced the largest effect on the calcium channel. The Journal of Physiology (1998) 1. Glutamate suppressed high-voltage-activated barium currents (IBa,HVA) in tiger salamander retinal ganglion cells. Both ionotropic (iGluR) and metabotropic (mGluR) receptors contributed to this calcium channel inhibition. 2. Trans-ACPD (1-aminocyclopentane-trans-1S,3R-dicarboxylic acid), a broad-spectrum metabotropic glutamate receptor agonist, suppressed a dihydropyridine-sensitive barium current. Kainate, an ionotropic glutamate receptor agonist, reduced an ù-conotoxin GVIAsensitive current. 3. The relative effectiveness of selective agonists indicated that the predominant metabotropic receptor was the l-2-amino-4-phosphonobutyrate (l-AP4)-sensitive, group III receptor. This receptor reversed the action of forskolin, but this was not responsible for calcium channel suppression. l_AP4 raised internal calcium concentration. Antagonists of phospholipase C, inositol trisphosphate (IP×) receptors and ryanodine receptors inhibited the action of metabotropic agonists, indicating that group III receptor transduction was linked to this pathway. 4. The action of kainate was partially suppressed by BAPTA, by calmodulin antagonists and by blockers of calmodulin-dependent phosphatase. Suppression by kainate of the calcium channel current was more rapid when calcium was the charge carrier, instead of barium. The results indicate that calcium influx through kainate-sensitive glutamate receptors can activate calmodulin, which stimulates phosphatases that may directly suppress voltage-sensitive calcium channels. 5. Thus, ionotropic and metabotropic glutamate receptors inhibit distinct calcium channels.They could act synergistically, since both increase internal calcium. These pathways provide negative feedback that can reduce calcium influx when ganglion cells are depolarized.7667

show abstract

Inositol 1,4,5-trisphosphate-induced Ca2+ release is regulated by cytosolic Ca2+ in intact skeletal muscle

Cited by 10 publications

References 42 publications

Rapid cooling-induced contractures in rat skinned skeletal muscle fibres originate from sarcoplasmic reticulum Ca2+ release through ryanodine and inositol trisphosphate receptors

Rapid cooling-induced contractures in rat skinned skeletal muscle fibres originate from sarcoplasmic reticulum Ca2+ release through ryanodine and inositol trisphosphate receptors

Increases in [IP3]i aggravates diastolic [Ca2+] and contractile dysfunction in Chagas’ human cardiomyocytes

Metabotropic and ionotropic glutamate receptors regulate calcium channel currents in salamander retinal ganglion cells

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