Mechanism(s) of the hypotensive effect of synthetic 1-O-octadecyl-2-O-acetyl-glycero-3-phosphorylcholine

Kamitani, Toshiharu; Katamoto, Michiyo; Tatsumi, Mitsuyoshi; Katsuta, Kiyotaka; Ono, Takaharu; Kikuchi, Hiroyuki; Kumada, Shigenobu

doi:10.1016/0014-2999(84)90284-x

Cited by 45 publications

(19 citation statements)

References 17 publications

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“…Levi et al (1984) demonstrated that AGEPC in concentrations of 1O-1-1O-M produced a slight negative inotropic effect in guinea-pig isolated left atria and papillary muscles. On the contrary, a positive inotropic effect of AGEPC at a concentration of l0-4 M in rat atria was reported from two laboratories a (Cervoni et al, 1983;Kamitani et al, 1984). In the light of the present observations, however, these reports may not be contradictory.…”

Section: Electrophysiological Effects Ofamphiphiles On Guineapigpapilcontrasting

confidence: 70%

“…Therefore, the electrophysiological effects of AGEPC might stem from non-specific amphiphile-membrane interaction rather than from activation of specific Paf receptors. It has been also reported that high concentrations (10-'-3 x 10-4 M) ofAGEPC were needed to induce mechanical responses in isolated vascular 40 mV preparations (Cervoni et al, 1983;Kamitani et al, 1984;Vanhoutte & Houston, 1985). Vanhoutte & Houston (1985) have suggested that the Paf-induced | 20 mg relaxation of the isolated coronary artery of the dog is not receptor-mediated, since the mechanical response was not blocked by a Paf-antagonist.…”

Section: Electrophysiological Effects Ofamphiphiles On Guineapigpapilmentioning

confidence: 98%

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Electrophysiological effects of acetyl glyceryl ether phosphorylcholine on cardiac tissues: comparison with lysophosphatidylcholine and long chain acyl carnitine

Nakaya

Tohse

1986

British J Pharmacology

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1 Electrophysiological effects of synthetic platelet activating factor, acetyl glyceryl ether phosphorylcholine (AGEPC), were examined and compared with those of lysophosphatidylcholine (LPC) and long chain acyl carnitine (AC) in canine Purkinje fibres and guinea-pig papillary muscles, by use of standard microelectrode techniques.2 In canine Purkinje fibres, AGEPC at concentrations higher than 3 x 10-5 M, decreased maximum diastolic potential, action potential amplitude and the maximum upstroke velocity ofphase 0. AGEPC also induced abnormal automaticity arising from depolarized membrane potentials.3 LPC and AC in concentrations higher than 3 x 1O-5M also produced virtually identical electrophysiological alterations in Purkinje fibres. 4 Although twitch tension was slightly decreased by low concentrations (10-6_1l-0M) of these amphiphilic lipids, a transient positive inotropic response appeared at the beginning of a progressive depolarization after exposure to higher concentrations of the amphiphiles. 5 In guinea-pig papillary muscles, AGEPC in concentrations higher than 3 x 10I-5 M produced slight decreases in resting membrane potential, action potential amplitude and action potential durations, concomitantly with a positive inotropic response. These electrophysiological and mechanical changes were also induced by LPC and AC at comparable concentrations.6 In guinea-pig papillary muscles depolarized with 25 mM [K']0, AGEPC, LPC and AC all evoked slow action potentials at a concentration of 10-'M. 7 It is concluded that in isolated cardiac tissues AGEPC exerts electrophysiological effects similar to those of LPC and AC only at high concentrations, and that the non-specific interaction of amphiphiles with sarcolemmal membrane may be responsible for the electrophysiological and mechanical effects.

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Section: Electrophysiological Effects Ofamphiphiles On Guineapigpapilcontrasting

confidence: 70%

Section: Electrophysiological Effects Ofamphiphiles On Guineapigpapilmentioning

confidence: 98%

Electrophysiological effects of acetyl glyceryl ether phosphorylcholine on cardiac tissues: comparison with lysophosphatidylcholine and long chain acyl carnitine

Nakaya

Tohse

1986

British J Pharmacology

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“…Also, PAF itself had direct negative inotropic effects (Tamargo et al, 1985;Robertson et al, 1988 (Toyofuku et al, 1988;Yamanaka et al, 1992), and leukotrienes (Piper & Stewart, 1986) in response to exogenous PAF have been observed. Several in vitro experiments (Kamitani et al, 1984;Kamata et al, 1989;Chiba et al, 1990;Moritoki et al, 1992;Juncos et al, 1993) have suggested the involvement of EDRF or NO in the vasodilator effects of PAF. In this study, we observed that, firstly, decreases in SVR seen immediately following the injection of PAF 0.25 jg kg-' were significantly inhibited by pretreatment with the NO synthase inhibitor L-NAME and also with the PAF antagonist TCV-309; secondly, decreases in mAoP and SVR induced by the lower dose of PAF (0.05 jg kg-') were significantly attenuated by another NO synthase inhibitor L-NNA; thirlly, these reduced effects of PAF produced by L-NNA were restored with administration of L-arginine, a substrate for NO synthase.…”

Section: Discussionmentioning

confidence: 99%

“…( Heffner et al, 1983;Piper & Stewart, 1986;Hu & Man, 1991), leukotrienes (Voelkel et al, 1982;Sybertz et al, 1985;Piper & Stewart, 1986) and PAF itself (Tessner et al, 1989). In addition, several lines of evidence indicate that production of endothelium-derived relaxing factor (EDRF), which is thought to be nitric oxide (NO; Palmer et al, 1987), may contribute to the vasodilator actions of PAF in in vitro preparations (Kamitani et al, 1984;Kamata et al, 1989;Chiba et al, 1990;Moritoki et al, 1992;Juncos et al, 1993). Nevertheless, the role of NO in PAF-induced hypotensive actions in in vivo exa 10 ,,-20 (R perimental models remains controversial (Filep & F6ldes-Filep, 1993;Takekoshi et al, 1993).…”

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confidence: 99%

Involvement of nitric oxide and eicosanoids in platelet‐activating factor‐induced haemodynamic and haematological effects in dogs

Noguchi

Matsuzaki

Shiroma

et al. 1996

British J Pharmacology

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1 Platelet-activating factor (PAF) is a phospholipid mediator with potent cardiovascular and haematological actions. But its mechanisms of action in vivo have not been fully elucidated, probably due to difficulties arising from previous findings that the effects of PAF are largely mediated by the release of a variety of other autacoids. In the present study, the roles of nitric oxide and eicosanoids in the effects of PAF (0.01 -0.25 pg kg-1 i.v.) on systemic and pulmonary vasculatures and circulating blood cell count were pharmacologically evaluated in anaesthetized dogs. 2 Higher doses of PAF (>0.1 yg kg-1) produced a biphasic systemic hypotension. The first hypotension seen 30 s after the injection was accompanied by a decrease in systemic vascular resistance, thrombocytopenia and leukopenia, while the second hypotension seen 1-2 min after PAF was accompanied by a marked rise in pulmonary vascular resistance and decreases in aortic blood flow and cardiac contractility. Lower doses of PAF (0.01-0.05 Mg kg-') caused only the first responses in a dosedependent manner. 3 Pretreatment with indomethacin inhibited the second responses to PAF without affecting the first responses. The thromboxane A2/prostaglandin H2 (TP)-receptor antagonist vapiprost blocked the PAFinduced rise in pulmonary vascular resistance. AA-861, a 5-lipoxygenase inhibitor, attenuated the PAFinduced cardiac depression. The nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester inhibited the PAF-induced early decrease in systemic vascular resistance. 4 All observed changes in haemodynamics and blood cell count after PAF were almost abolished by TCV-309, a PAF-receptor antagonist. 5 Reproducible hypotension and thrombocytopenia produced by a lower dose of PAF (0.05 Mg kg-1) were respectively attenuated and potentiated by pretreatment with NG-nitro-L-arginine, another nitric oxide synthase inhibitor. Administration of L-arginine reversed the effects of the nitric oxide synthase inhibitor. 6 These results indicate that PAF-receptor-mediated production of not only eicosanoids but also nitric oxide may contribute to the cardiovascular and haematological responses to PAF in the dog.

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“…The coronary vascular response was not related temporally to the relatively small negative inotropic response observed in the region of distribution of the LCX coronary artery. A positive inotropic response to AGEPC has been noted in rat atrial preparations (Kamitani et al, 1984), whereas Levi et al (1984) have reported that AGEPC administered to the guinea pig-perfused heart resulted in a marked 43 ± 7f 43±8t 4 ±2% 3 ±2…”

Section: Discussionmentioning

confidence: 99%

Platelet-activating factor and the release of a platelet-derived coronary artery vasodilator substance in the canine.

Jackson

Schumacher

Kunkel³

et al. 1986

Circulation Research

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which is released by stimulated neutrophils and platelets, possesses the ability to alter vascular tone and permeability and to activate various formed blood elements. We have characterized the hemodynamic effects of intracoronary injections of plateletactivating factor and the influences of pharmacological blockade and platelet depletion on its activity. Intracoronary injections of platelet-activating factor produced maximum increases in left circumflex coronary artery blood flow of 55 ± 8, 52 ± 8, and 52 ± 7 ml/min at 0.5, 1.0, and 2.0 nM, respectively. Only modest changes in systemic arterial blood pressure and regional developed isometric contractile force were associated with the intracoronary artery administration of platelet-activating factor over the range of doses studied. The increase in left circumflex coronary artery blood flow in response to platelet-activating factor was attenuated (44%), but not prevented, by pretreatment with diphenhydramine, (4 mg/kg, iv), and was not affected by pretreatment with aspirin (20 mg/kg, iv) or the systemic administration of the serotonin receptor antagonist, methysergide. The coronary vasodilator response to platelet-activating factor was reduced significantly by the induction of thrombocytopenia (95 ± 3% platelet depletion) through the administration of sheep-derived canine platelet antiserum. The intracoronary artery injection of platelet-rich plasma activated with platelet-activating factor into thrombocytopenic dogs produced a significantly greater increase in coronary artery blood flow than the injection of either non-activated platelet-rich plasma or platelet-depleted plasma to which platelet-activating factor was added. Similar changes in coronary artery blood flow could be obtained with the intracoronary artery injection of cell-free supernates from washed platelets activated with platelet-activating factor. The observed results suggest that circulating platelets, when exposed to platelet-activating factor, can release a coronary dilator substance, and that the coronary artery dilation is not prevented by pharmacological receptor antagonists for histamine, serotonin, or inhibitors of cyclooxygenase. (CircRes 58: 218-229, 1986)

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Mechanism(s) of the hypotensive effect of synthetic 1-O-octadecyl-2-O-acetyl-glycero-3-phosphorylcholine

Cited by 45 publications

References 17 publications

Electrophysiological effects of acetyl glyceryl ether phosphorylcholine on cardiac tissues: comparison with lysophosphatidylcholine and long chain acyl carnitine

Electrophysiological effects of acetyl glyceryl ether phosphorylcholine on cardiac tissues: comparison with lysophosphatidylcholine and long chain acyl carnitine

Involvement of nitric oxide and eicosanoids in platelet‐activating factor‐induced haemodynamic and haematological effects in dogs

Platelet-activating factor and the release of a platelet-derived coronary artery vasodilator substance in the canine.

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