Inositol 1,4,5‐trisphosphate and 5′‐GTP induce calcium release from different intracellular pools

Henne, Volkmar; Piiper, Albrecht; Söling, Hans‐Dieter

doi:10.1016/0014-5793(87)81037-2

Cited by 69 publications

(24 citation statements)

References 12 publications

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“…In Swiss 3T3 fibroblasts, the bombesinor vasopressin-stimulated elevation of [Ca2+]i was mediated by an increase in the production of 1,4,5-InsP s, while the platelet-derived growth factor-induced eleva-tion of [Ca~+] i was not (Lopez-Rivas et al, 1987). Other reports demonstrated that (intracellular) GTP can release Ca 2+ from different intracellular pools insensitive to InsP 3 (Henne et al, 1987;Nicchitta et al, 1987;Benedetti et al, 1988), and that elevated concentrations of cytosolic Na + can exchange for mitochondrial Ca ~+. Similar pathways may be activated by ATP, although there is not yet any evidence for a specific mechanism.…”

Section: Extraceuular Ca 2+ Contributes To the Elevation Of [Ca2+]i Bmentioning

confidence: 96%

Effects of extracellular ATP on ion transport systems and [Ca2+]i in rat parotid acinar cells. Comparison with the muscarinic agonist carbachol.

Soltoff

McMillian

Cragoe

et al. 1990

The Journal of General Physiology

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The effects of extracellular ATP on ion fluxes and the intracellular free Ca 2 § concentration ([Ca~+]i) were examined using a suspension of rat parotid acinar cells and were contrasted with the effects of the muscarinic agonist carbachol. Although ATP and carbachol both rapidly increased [Ca2+] i about threefold above the resting level (200-250 nM), the effect of ATP was due primarily to an influx of Ca ~+ across the plasma membrane, while the initial response to carbachol was due to a release of Ca ~ § from intracellular stores. Within 10 s, ATP (1 mM) and carbachol (20 #M) reduced the cellular C1-content by 39-50% and cell volume by 15-25%. Both stimuli reduced the cytosolic K + content by 57-65%, but there were marked differences in the rate and pattern of net K § movement as well as the effects of K + channel inhibitors on the effluxes initiated by the two stimuli. The maximum rate of the ATP-stimulated K § efflux (~2,200 nmol K+/mg protein per min) was about two-thirds that of the carbachol-initiated efflux rate, and was reduced by ~30% (vs. 60% for the carbachol-stimulated K + efflux) by TEA (tetraethylammonium), an inhibitor of the large conductance (BK) K § channel. Charybdotoxin, another K § channel blocker, was markedly more effective than TEA on the effects of both agonists, and reduced the rate of K § effiux initiated by both ATP and carbachol by ~80%. The removal of extracellular Ca ~ § reduced the ATPand the carbachol-stimulated rates of K + efflux by 55 and 17%, respectively. The rate of K + effiux initiated by either agonist was reduced by 78-95% in cells that were loaded with BAPTA to slow the elevation of [Ca2+]i. These results indicated that ATP and carbachol stimulated the effiux of K + through multiple types of K § permeable channels, and demonstrated that the relative proportion of efflux 320THE JOURNAL OF GENERAL PHYSIOLOGY 9 VOLUME 95 9 1990 through the different pathways was different for the two stimuli. ATP and carbachol also stimulated the rapid entry of Na § into the parotid cell, and elevated the intracellular Na § content to 4.4 and 2.6 times the normal level, respectively. The rate of Na § entry through Na+-K+-2CI-cotransport and Na+-H § exchange was similar whether stimulated by ATP, carbachol, or ionomycin, and uptake through these two carrier-mediated transporters accounted for 50% of the ATP-promoted Na § influx. The remainder may be due to a nonselective cation channel and an ATP-gated cation channel that is also permeable to Ca ~ § The consumption of extracellular ATP by an ecto-ATPase (apparent K0.5 for ATP is 0.93 mM) on the plasma membrane limited the duration of the response to ATP when large concentrations of cells were used. The effects of ATP on [Ca~+]i and ion fluxes were blocked specifically by DIDS (4,4'-diisothiocyanostilbene-2,2'-disulfonic acid), and were more potent in the absence of Mg ~+, suggesting that the active nucleotide moiety was ATP 4-. These studies suggest that ATP may function as a neurotransmitter and modulate fluid secretion by stimula...

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Section: Extraceuular Ca 2+ Contributes To the Elevation Of [Ca2+]i Bmentioning

confidence: 96%

Effects of extracellular ATP on ion transport systems and [Ca2+]i in rat parotid acinar cells. Comparison with the muscarinic agonist carbachol.

Soltoff

McMillian

Cragoe

et al. 1990

The Journal of General Physiology

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“…Inositol trisphosphate is formed at the basolateral membrane by receptor-ligand activation of phospholipase C hydrolysis of phosphatidylinositol 4,5-bisphosphate (9,12,(36)(37)(38)(39)(40). In many cell types (41), including the parotid acinar cell (13,42), inositol trisphosphate-induced Ca2+ release is associated with a microsomal fraction enriched in endoplasmic reticulum markers. Whether the entire endoplasmic reticulum, only a specialized fraction of it (35,(42)(43)(44)(45)(46)(47), or another organelle (48) …”

Section: Methodsmentioning

confidence: 99%

“…In many cell types (41), including the parotid acinar cell (13,42), inositol trisphosphate-induced Ca2+ release is associated with a microsomal fraction enriched in endoplasmic reticulum markers. Whether the entire endoplasmic reticulum, only a specialized fraction of it (35,(42)(43)(44)(45)(46)(47), or another organelle (48) …”

Section: Methodsmentioning

confidence: 99%

Physiological localization of an agonist-sensitive pool of Ca2+ in parotid acinar cells.

Foskett¹,

Gunter-Smith²,

Melvin³

et al. 1989

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

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The localized increase cannot be detected by fura-2 but is sufficient to open the Ca2+-sensitive K+ channels located in the basolateral membrane. We concluded that a receptormobilized intracellular store of Ca2+ is localized at or near the basolateral membrane.Fluid secretion by mammalian exocrine cells, including salivary acinar cells, is regulated by alterations in plasma membrane ion permeabilities (1). Among the earliest events associated with agonist-induced stimulation offluid secretion are a rapid plasma membrane hyperpolarization (1-4) and a dramatic loss of cellular K+ (5). Patch-clamp studies have identified Ca2+-and voltage-sensitive K+ channels in salivary and pancreatic acinar basolateral membranes whose activation by secretagogues is believed to underlie these effects (6). Another early event associated with agonist stimulation is a rapid rise in the level of intracellular free calcium ([Ca2+]i) (7-11). As in a wide variety of other cell types, [Ca2+]i is thought to rise as a result of inositol trisphosphate mobilization of intracellular stores (9,12,13), as well as enhanced Ca2+ influx across the plasma membrane (7,(14)(15)(16)(17). A large body of evidence indicates that the rise of [Ca2+]J is directly responsible for activating the K+ channels in the acinar basolateral membranes. Specifically, it has been shown that (i) the Ca2+ sensitivity of the K+ channels is within the appropriate physiological (agonist-induced) range of [Ca2+]J (6, 18-21),(ii) the cellular K+ loss is abolished in Ca2+-depleted cells stimulated in Ca2+-free medium (22, 23), (iii) the application of Ca2" ionophores to acinar cells activates K+ channels and causes a loss of cellular K+ similar to that caused by agonists (23-26), (iv) the intracellular perfusion of a Ca2+ chelator blocks the agonist-stimulated increase in K+ conductance (18,26,27), and (v) the intracellular perfusion of inositol trisphosphate activates the K+ conductance (28).One aspect that has not yet been explored, however, is the temporal relationship between the agonist-induced rise of (29). In the present study, we examine the relationship between the agonist-induced rise of [Ca2+] (measured with the Ca2+-sensitive fluorescent dye fura-2) and membrane K+ conductance (measured simultaneously with an intracellular microelectrode) in rat parotid acinar cells. The data indicate that a receptor-mobilized store of Ca2+ is localized at or near the basolateral membrane.

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“…the ER or selectively from one portion (Henne et al, 1987;Daniell and Harris, 1989;Ghosh et al, 1989;Burgoyne, et al, 1989), nor is it established whether the ER calcium pump is distributed uniformly or heterogeneously throughout the brain. Release of calcium by IP3 is mediated by a specific receptor protein which has been localized in the brain by autoradiography (Worley et al, 1987a(Worley et al, , 1989 and immunohistochemistry (Ross et al, 1989a), purified to homogeneity (Supattapone et al, 1988), molecularly cloned (Furuichi et al, 1989), and shown to comprise within a four-subunit 1000-kD protein both the IP3 recognition site and its associated calcium channel (Ferris et al, 1989).…”

Section: Introductionmentioning

confidence: 99%

Rat brain endoplasmic reticulum calcium pools are anatomically and functionally segregated.

et al. 1990

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Autoradiographic imaging can localize 45Ca2+ selectively accumulated via the Ca2+, Mg2(+)-ATPase into endoplasmic reticulum stores in rat brain slices. 45Ca2+ accumulation is markedly stimulated by oxalate and displays a heterogeneous distribution which resembles the mRNA distribution for a sarcoendoplasmic reticulum Ca2+, Mg2(+)-ATPase. Inositol 1,4,5-triphosphate [I(1,4,5)P3] inhibits 45Ca2+ accumulation selectively into regions corresponding to those enriched in I(1,4,5)P3 receptor-binding sites and in Ca2+, -Mg2(+)-ATPase mRNA. Thus rat brain endoplasmic reticulum calcium stores are anatomically and functionally differentiated.

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Inositol 1,4,5‐trisphosphate and 5′‐GTP induce calcium release from different intracellular pools

Cited by 69 publications

References 12 publications

Effects of extracellular ATP on ion transport systems and [Ca2+]i in rat parotid acinar cells. Comparison with the muscarinic agonist carbachol.

Effects of extracellular ATP on ion transport systems and [Ca2+]i in rat parotid acinar cells. Comparison with the muscarinic agonist carbachol.

Physiological localization of an agonist-sensitive pool of Ca2+ in parotid acinar cells.

Rat brain endoplasmic reticulum calcium pools are anatomically and functionally segregated.

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