Stimulation of calcium uptake in platelet membrane vesicles by adenosine 3′,5′-cyclic monophosphate and protein kinase

Käser-Glanzmann, R.; Jakábová, Milica; George, JN; Lüscher, E. F.

doi:10.1016/0005-2736(77)90336-4

Cited by 299 publications

(67 citation statements)

References 30 publications

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“…The anti-aggregating actions of prostacyclin and NO are potentiated by HL 725 and M & B 22948 respectively. Cyclic AMP is thought to regulate calcium levels by promoting its uptake into the dense tubular system (Kaser-Glanzmann et al, 1977) and cyclic GMP by inhibiting calcium influx and mobilization from intracellular stores . Therefore the final common step in the inhibition of platelet aggregation by prostacyclin and NO is likely to be calcium availability.…”

Section: Discussionmentioning

confidence: 99%

Comparative pharmacology of endothelium‐derived relaxing factor, nitric oxide and prostacyclin in platelets

Radomski

Palmer

Moncada

1987

British J Pharmacology

785

295

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The pharmacological effects of endothelium‐derived relaxing factor (EDRF), nitric oxide (NO) and prostacyclin on human and rabbit platelets were examined. EDRF is released from porcine aortic endothelial cells, cultured on microcarriers and treated with indomethacin, in sufficient quantities to inhibit platelet aggregation induced by 9,11‐dideoxy‐9α,11α‐methano epoxy‐prostaglandin F2α (U46619) and collagen. The anti‐aggregating activity of EDRF was potentiated by M&B 22948, a selective inhibitor of cyclic GMP phosphodiesterase, and by superoxide dismutase (SOD) and was inhibited by haemoglobin and Fe2+. Both NO and prostacyclin inhibited platelet aggregation. The anti‐aggregatory activity of NO, but not that of prostacyclin, was potentiated by M&B 22948 and by SOD and was inhibited by haemoglobin and Fe2+. Thus NO is a potent inhibitor of platelet aggregation whose activity on platelets mimics that of EDRF. It is likely that the inhibitory effect of NO on platelets represents the action of endogenous EDRF and therefore this substance, together with prostacyclin, is a regulator of platelet‐vessel wall interactions.

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Section: Discussionmentioning

confidence: 99%

Comparative pharmacology of endothelium‐derived relaxing factor, nitric oxide and prostacyclin in platelets

Radomski

Palmer

Moncada

1987

British J Pharmacology

785

295

View full text Add to dashboard Cite

show abstract

“…In contrast to TXA2 it enhances Ca + sequestration (KazerGlanzman, Jakabova, George & Luscher, 1977). Moreover, inhibitory effects on platelet phospholipase (Lapetina, Schmitges, Chandrabose & Cuatrecasas, 1977;Minkes, Stanford, Chi, Roth, Raz, Needleman & Majerus, 1977) and platelet cyclo-oxygenase have been described (Malmsten, Granstrom & Samuelsson, 1976).…”

Section: Mechanism Of Actionmentioning

confidence: 99%

Eighth Gaddum Memorial Lecture University of London Institute of Education December 1980: Biological Importance of Prostacyclin

Moncada¹

1982

British J Pharmacology

266

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“…Consequently, how, and if, Ca2+ efflux from platelets can be modulated by processes regulated by CAMP, cGMP or DAG remains an enigma. The major intracellular organelle implicated in Ca2+ sequestration is the dense tubular system, and CAMP is known to promote accumulation of Ca2+ by this organelle [8]. The qualitatively similar effects elicited by NaNP and PMA would suggest that cGMP and DAG also promote Ca2+ sequestration in the dense tubular system.…”

Section: Methodsmentioning

confidence: 97%

Regulation of platelet cytosolic free calcium by cyclic nucleotides and protein kinase C

1985

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PAF elicits a rapid, concentration-dependent elevation of platelet cytosolic free calcium ([Car]), measured by quin2. Elevation of [Car] is transient, and the rate of reversal increases with agonist concentration. Adenylate cyclase stimulants (PGI,, PGDJ and 8-bromo CAMP; a guanylate cyclase stimulant (sodium nitroprusside) and 8-bromo cGMP; and a protein kinase C stimulant (phorbol myristate acetate) block the elevation of [Car] induced by PAF, and accelerate its reversal. These results suggest that CAMP, cGMP and 1,2-diacylglycerol (DAG) could act as second messengers to regulate [Car] in platelets. As PAF is known to stimulate platelet phosphoinositide hydrolysis (ergo DAG formation) but fails to elevate platelet CAMP or cGMP. it is proposed that DAG, via activation of protein kinase C, may act as an endogenous modulator of platelet [Car]: an action that contributes to the role of DAG as a bi-directional regulator of platelet reactivity.

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Stimulation of calcium uptake in platelet membrane vesicles by adenosine 3′,5′-cyclic monophosphate and protein kinase

Cited by 299 publications

References 30 publications

Comparative pharmacology of endothelium‐derived relaxing factor, nitric oxide and prostacyclin in platelets

Comparative pharmacology of endothelium‐derived relaxing factor, nitric oxide and prostacyclin in platelets

Eighth Gaddum Memorial Lecture University of London Institute of Education December 1980: Biological Importance of Prostacyclin

Regulation of platelet cytosolic free calcium by cyclic nucleotides and protein kinase C

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