Morphine antagonises prostaglandin E1- mediated inhibition of human platelet aggregation

Gryglewski, Ryszard J.; Szczeklik, Andrzej; Bieroń, K

doi:10.1038/256056a0

Cited by 40 publications

(13 citation statements)

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“…In 1975, Gryglewski et al [32] described a reversal of the prostaglandin (PGEi) inhibi tion of human platelet aggregation by mor phine in pharmacological concentrations, but this could not be confirmed by Reches et al [72]. After trying to find specific binding of 3H-elorphine, the latter group concluded that the presence of opiate receptors in human platelets 'is unlikely'.…”

Section: Platelets or Thrombocytesmentioning

confidence: 99%

Β-Endorphin Modulates Immune Functions

Fischer¹,

Falke²

1984

Psychother Psychosom

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Section: Platelets or Thrombocytesmentioning

confidence: 99%

Β-Endorphin Modulates Immune Functions

Fischer¹,

Falke²

1984

Psychother Psychosom

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“…In addition, they are present in some human blood ceils, i.e. erythrocytes [5], T lymphocytes [6], and neutrophils and monocytes [7], whereas their presence in human platelets [8] has been questioned [9].…”

Section: Introductionmentioning

confidence: 99%

Histamine release from isolated rat mast cells induced by opiates: effect of sterical configuration and calcium

Grosman

Jensen

1982

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The stereospecificity of the action of opiates on rat mast cells was investigated by means of the l- and d-isomers levorphanol and dextrorphan. The dose-response curves for histamine release induced by the 2 drugs were of a similar shape with a maximum at 2 X 10(-3) M and a pronounced minimum at 5 X 10(-3) M. At concentrations below 5 X 10(-3) M the effect of both drugs resembled that of morphine, i.e. the release occurred rapidly and inhibition was observed with naloxone, codeine, and antimycin A. Levorphanol, dextrorphan, and the antagonist levallorphan at concentrations above 5 X 10(-3) M seemed to be toxic to mast cells. The uptake of 45Ca in connection with histamine release induced by pethidine, levorphanol, and dextrorphan was lower than that of control cells, whereas the uptake induced by morphine did not differ from that of controls. The inhibition of compound 48/80-induced histamine release by morphine was paralleled by a reduced 45Ca uptake. The time course for the inhibitory effect of preincubation with morphine was similar for the histamine released induced by morphine and by compound 48/80. Washing of the cells after preincubation with morphine was without effect on the inhibition of morphine-induced histamine release, whereas the inhibition of compound 48/80 was reduced. The present observation with morphine and compound 48/80 support our previous impression of similarities in their mode of action, but a mechanism implying an interference by morphine with the disposition of calcium could also account for the findings. The observed antagonism between morphine and calcium resembles that of opiate receptors, but histamine release induced by opiates does not involve stereospecific opiate receptors.

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“…On the other hand, studies of the effects of morphine on platelets are relatively rarely compared with studies of its effects on blood vessels. Gryglewski et al [10] presented data to indicate that morphine antagonizes prostaglandin E 1 (PGE 1 )-mediated inhibition of human platelet aggregation; the antagonism between PGE 1 and morphine is similar to that described in rat brain homogenate and has also been demonstrated in human platelets [7]. They also speculated that adenylate cyclase may be the common target for PGE 1 and morphine in platelets as it is in neurons [7].…”

Section: Introductionmentioning

confidence: 90%

“…Gryglewski et al [10] showed that morphine inhibits the anti-aggregating effect of PGE 1 on ADP-and adrenaline-induced platelet aggregation, and suggested that the inhibition by morphine is mediated through platelet adenylate cyclase activity. Local interactions between · 2 -adrenoceptors and an opioid agonist or antagonist have been reported [9,24].…”

Section: Discussionmentioning

confidence: 99%

Morphine-Potentiated Platelet Aggregation in in vitro and Platelet Plug Formation in in vivo Experiments

et al. 2003

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The detailed mechanisms underlying morphine-signaling pathways in platelets remain obscure. Therefore, we systematically examined the influence of morphine on washed human platelets. In this study, washed human platelet suspensions were used for in vitro studies. Furthermore, platelet thrombus formation induced by irradiation of mesenteric venules with filtered light in mice pretreated with fluorescein sodium was used for an in vivo thrombotic study. Morphine concentration dependently (0.6, 1, and 5 µM) potentiated platelet aggregation and the ATP release reaction stimulated by agonists (i.e., collagen and U46619) in washed human platelets. Yohimbine (0.1 µM), a specific α₂-adrenoceptor antagonist, markedly abolished the potentiation of morphine in platelet aggregation stimulated by agonists. Morphine also potentiated phosphoinositide breakdown and intracellular Ca²⁺ mobilization in human platelets stimulated by collagen (1 µg/ml). Moreover, morphine (0.6–5 µM) markedly inhibited prostaglandin E₁ (10 µM)-induced cyclic AMP formation in human platelets, while yohimbine (0.1 µM) significantly reversed the inhibition of cyclic AMP by morphine (0.6 and 1 µM) in this study. The thrombin-evoked increase in pH_i was markedly potentiated in the presence of morphine (1 and 5 µM). Morphine (2 and 5 mg/g) significantly shortened the time require to induce platelet plug formation in mesenteric venules. We concluded that morphine may exert its potentiation in platelet aggregation by binding to α₂-adrenoceptors in human platelets, with a resulting inhibition of adenylate cyclase, thereby reducing intracellular cyclic AMP formation followed by increased activation of phospholipase C and the Na⁺/H⁺ exchanger. This leads to increased intracellular Ca²⁺ mobilization, and finally potentiation of platelet aggregation and of the ATP release reaction.

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Morphine antagonises prostaglandin E1- mediated inhibition of human platelet aggregation

Cited by 40 publications

References 13 publications

Β-Endorphin Modulates Immune Functions

Β-Endorphin Modulates Immune Functions

Histamine release from isolated rat mast cells induced by opiates: effect of sterical configuration and calcium

Morphine-Potentiated Platelet Aggregation in in vitro and Platelet Plug Formation in in vivo Experiments

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