Actions of PGE2 and indomethacin on adrenergic neuroeffector transmission in the rabbit coeliac artery

B. Malomvolgyi, Zs Bunyevacz, P. Hadhazy, K. Magyar

Research output: Contribution to journalArticle

Abstract

In the present study we have investigated the pre- and post-synaptic actions of PGE2 and indomethacin on the adrenergic transmission in isolated coeliac arteries of rabbits. The artery segment was preloaded with (3H)NA and suspended in an organ bath (37°C, 5% CO2 - 95% O2, isometric recording). The preparation was superfused with Krebs-solution containing the uptake blockers cocaine and corticosterone. To release neurotransmitter, the artery was stimulated by electrical square-wave pulses (0.5 ms, 5 Hz, 60 s) using platinum wire electrodes. The perfusate was collected in 3 or 6 min samples. The outflow of labelled neurotransmitter was expressed in pmol/3 min. Inhibition of endogenous prostaglandin-biosynthesis by indomethacin (3 μmol/l) potentiated the contractile responses to nerve stimulation (57±15%, n=4), but did not influence the release of NA (the release ratio was 1.02±0.03, n=4). The endogenous prostaglandins may modulate vascular neuroeffector transmission postjunctionally, because cyclooxygenase inhibition did not cause any change in transmitter release. The effects of exogenous PGE2 on adrenergic transmission and contraction were also studied. In this case, indomethacin was present to minimize the potential complicating actions of endogenous prostanoids. At low concentrations (1, 3 and 10 nmol/l) PGE2 dose-dependently inhibited vasocontrictor responses to nerve stimulation (IC50=4.7±1.5 nmol/l, n=4), but was ineffective in influencing transmitter release (the stimulation evoked release ratios were 0.95±0.05, 1.00±0.08 and 0.93±0.11, n=4, respectively). It may be concluded, therefore, that PGE2, at least in the concentrations tested, had no effect on the release of NA, indicating that the effect of this prostanoid was postjunctional.

Original languageEnglish
JournalBiomedica Biochimica Acta
Volume47
Issue number10-11
Publication statusPublished - 1988

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Celiac Artery
Dinoprostone
Indomethacin
Adrenergic Agents
Prostaglandins
Rabbits
Neurotransmitter Agents
Transmitters
Arteries
Biosynthesis
Prostaglandin-Endoperoxide Synthases
Corticosterone
Platinum
Baths
Cocaine
Action Potentials
Inhibitory Concentration 50
Blood Vessels
Electrodes
Wire

ASJC Scopus subject areas

  • Biochemistry

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Actions of PGE2 and indomethacin on adrenergic neuroeffector transmission in the rabbit coeliac artery. / Malomvolgyi, B.; Bunyevacz, Zs; Hadhazy, P.; Magyar, K.

In: Biomedica Biochimica Acta, Vol. 47, No. 10-11, 1988.

Research output: Contribution to journalArticle

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abstract = "In the present study we have investigated the pre- and post-synaptic actions of PGE2 and indomethacin on the adrenergic transmission in isolated coeliac arteries of rabbits. The artery segment was preloaded with (3H)NA and suspended in an organ bath (37°C, 5{\%} CO2 - 95{\%} O2, isometric recording). The preparation was superfused with Krebs-solution containing the uptake blockers cocaine and corticosterone. To release neurotransmitter, the artery was stimulated by electrical square-wave pulses (0.5 ms, 5 Hz, 60 s) using platinum wire electrodes. The perfusate was collected in 3 or 6 min samples. The outflow of labelled neurotransmitter was expressed in pmol/3 min. Inhibition of endogenous prostaglandin-biosynthesis by indomethacin (3 μmol/l) potentiated the contractile responses to nerve stimulation (57±15{\%}, n=4), but did not influence the release of NA (the release ratio was 1.02±0.03, n=4). The endogenous prostaglandins may modulate vascular neuroeffector transmission postjunctionally, because cyclooxygenase inhibition did not cause any change in transmitter release. The effects of exogenous PGE2 on adrenergic transmission and contraction were also studied. In this case, indomethacin was present to minimize the potential complicating actions of endogenous prostanoids. At low concentrations (1, 3 and 10 nmol/l) PGE2 dose-dependently inhibited vasocontrictor responses to nerve stimulation (IC50=4.7±1.5 nmol/l, n=4), but was ineffective in influencing transmitter release (the stimulation evoked release ratios were 0.95±0.05, 1.00±0.08 and 0.93±0.11, n=4, respectively). It may be concluded, therefore, that PGE2, at least in the concentrations tested, had no effect on the release of NA, indicating that the effect of this prostanoid was postjunctional.",
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