Inositol 1,4,5-trisphosphate releases Ca2+ from intracellular store sites in skinned single cells of porcine coronary artery

Suematsu, Eiichi; Hirata, Masato; Hashimoto, Toshihiko; Kuriyama, Hirosi

doi:10.1016/0006-291x(84)91279-8

Cited by 370 publications

(104 citation statements)

References 10 publications

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“…Soon after the first report of IP 3 -evoked Ca 2þ release, cytosolic Ca 2þ was shown also to regulate IP 3 R (Suematsu et al 1984;Jean and Klee 1986); thereafter, it emerged that the effects of Ca 2þ were biphasic, with modest increases in cytosolic Ca 2þ concentration enhancing responses to IP 3 , while higher concentrations were inhibitory (Iino 1987;Iino 1990;Finch et al 1991;Parys et al 1992;Marshall and Taylor 1993). This provided yet another parallel with RyR, which are also biphasically regulated by Ca 2þ (Hamilton 2005).…”

Section: Regulation Of Ip 3 Receptors By Ca 2þ and Ipmentioning

confidence: 99%

IP3 Receptors: Toward Understanding Their Activation

Taylor¹,

Tovey²

2010

Cold Spring Harbor Perspectives in Biology

259

190

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Inositol 1,4,5-trisphosphate receptors (IP 3 R) and their relatives, ryanodine receptors, are the channels that most often mediate Ca 2þ release from intracellular stores. Their regulation by Ca 2þ allows them also to propagate cytosolic Ca 2þ signals regeneratively. This brief review addresses the structural basis of IP 3 R activation by IP 3 and Ca 2þ . IP 3 initiates IP 3 R activation by promoting Ca 2þ binding to a stimulatory Ca 2þ -binding site, the identity of which is unresolved. We suggest that interactions of critical phosphate groups in IP 3 with opposite sides of the clam-like IP 3 -binding core cause it to close and propagate a conformational change toward the pore via the adjacent N-terminal suppressor domain. The pore, assembled from the last pair of transmembrane domains and the intervening pore loop from each of the four IP 3 R subunits, forms a structure in which a luminal selectivity filter and a gate at the cytosolic end of the pore control cation fluxes through the IP 3 R.

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Section: Regulation Of Ip 3 Receptors By Ca 2þ and Ipmentioning

confidence: 99%

IP3 Receptors: Toward Understanding Their Activation

Taylor¹,

Tovey²

2010

Cold Spring Harbor Perspectives in Biology

259

190

View full text Add to dashboard Cite

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“…Ca from the sarcoplasmic reticulum in the presence or absence of ex tracellular Ca (6,11,(20)(21)(22)(23). The effects of E-4701 or nitroglycerin on the rabbit endo thelium-denuded mesenteric artery were in vestigated with regard to the contraction evoked by NA in Ca-free solution (Fig.…”

Section: Resultsmentioning

confidence: 93%

“…InsP3 synthesized by NA in the mesenteric artery and by ACh in the coronary artery pro duced a contraction due to an increase in the free Ca released from cellular stores (20)(21)(22)(23)31), and Ca influxes by activations of re ceptor operated Ca channels or/with the subsequently activated voltage dependent Ca channels by depolarization of the mem brane due to activations of receptor operated nonselective cation channels (32)(33)(34). On the other hand, high K activated the voltage dependent Ca channel.…”

Section: Discussionmentioning

confidence: 99%

Actions of a newly synthesized nitro-compound, E-4701, on rabbit vascular smooth muscles.

et al. 1989

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“…2). It has been reported that activation of a 1-adrenergic receptors by NE stimulates phosphoinositides turnover to increase the concentration of inositol trisphos phate and subsequently release the intracellu lar Ca 2+ store to mediate the phasic contrac tion (27,28). However, NE-induced inositol monophosphate formation was not affected by protopine, and this rules out that protopine may inhibit NE-induced phasic contraction through inhibition of NE-induced phosphoino sitides hydrolysis.…”

Section: Effects Of Protopine On Camp and Cgmp Formationmentioning

confidence: 96%

Ca2+-Channel Blockade in Rat Thoracic Aorta by Protopine Isolated from Corydalis Tubers.

Ko¹,

Wu²,

Lu³

et al. 1992

Jpn.J.Pharmacol

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ABSTRACT-The pharmacological properties and mechanism of the action of pro topine on isolated rat thoracic aorta were examined. It inhibited norepinephrine (NE, 3 ,uM)-induced tonic contraction in rat thoracic aorta in a concentration-dependent manner (25 100 ,ug/ml). The phasic contraction caused by NE was inhibited only by a high concentration of protopine (100pg/ml). At the plateau of NE-induced tonic contraction, the addition of protopine also caused relaxation. This relaxing effect of protopine was not antagonized by indomethacin (20,uM) or methylene blue (50,UM), and it still existed in denuded rat aorta or in the presence of nifedipine (2 100 ,u M). Protopine also inhibited high potassium (60 mM)-induced, calcium-dependent (0.03 3 mM) contraction of rat aorta in a concentration-dependent manner. Neither cAMP nor cGMP level was changed by protopine. Both the formation of inositol monophos phate caused by NE and the phasic contraction induced by caffeine were also not affected by protopine. 45Ca2+ influx caused by either NE or K+ was inhibited by protopine concentration-dependently. It is concluded that protopine relaxed the rat thoracic aorta mainly by suppressing the Ca 2+ influx through both voltage and receptor-operated calcium channels. Chemical structure of protopine.

show abstract

Inositol 1,4,5-trisphosphate releases Ca2+ from intracellular store sites in skinned single cells of porcine coronary artery

Cited by 370 publications

References 10 publications

IP3 Receptors: Toward Understanding Their Activation

IP3 Receptors: Toward Understanding Their Activation

Actions of a newly synthesized nitro-compound, E-4701, on rabbit vascular smooth muscles.

Ca2+-Channel Blockade in Rat Thoracic Aorta by Protopine Isolated from Corydalis Tubers.

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