Modulation by prostaglandins of the release of [3H]noradrenaline evoked by potassium and nerve stimulation in the isolated rat heart

Mohammad T. Khan, Kafait Malik

Research output: Contribution to journalArticle

24 Citations (Scopus)

Abstract

In the isolated rat heart perfused with Krebs solution and prelabeled with [3H]noradrenaline, we examined the effect of prostaglandins (PG) I2, E2, 6-keto-PGF and their precursor, arachidonic acid, on the overflow of tritium elicited by potassium (K+) and by stimulation of cardiac sympathetic nerve plexus. Prostaglandins E2, I2 and arachidonic acid but not 6-keto-PGF reduced K+ and nerve stimulation-induced overflow of tritium. Administration of indomethacin, an inhibitor of cyclooxygenase, increased tritium overflow elicited by either K+ or by nerve stimulation. During infusion of indomethacin, the inhibitory effect of both PGE2 and PGI2 on the K+ or nerve stimulation-induced overflow of tritium remained unaltered. In contrast, the effect of arachidonic acid to reduce K+ or nerve stimulation-induced overflow of tritium was abolished by indomethacin, indicating that the fatty acid inhibits release of tritium by its conversion to a product(s) of cyclooxygenase, presumably PGI2 and PGE2. These data suggest that prostaglandins, particularly PGI2 and PGE2 sythesized in the isolated rat heart act on prejunctional sites to modulate release of the adrenergic transmitter.

Original languageEnglish (US)
Pages (from-to)213-218
Number of pages6
JournalEuropean Journal of Pharmacology
Volume78
Issue number2
DOIs
StatePublished - Feb 26 1982

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Tritium
Prostaglandins
Epoprostenol
Norepinephrine
Potassium
Dinoprostone
Arachidonic Acid
Indomethacin
Cyclooxygenase Inhibitors
Prostaglandin-Endoperoxide Synthases
Adrenergic Agents
Fatty Acids

All Science Journal Classification (ASJC) codes

  • Pharmacology

Cite this

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abstract = "In the isolated rat heart perfused with Krebs solution and prelabeled with [3H]noradrenaline, we examined the effect of prostaglandins (PG) I2, E2, 6-keto-PGF1α and their precursor, arachidonic acid, on the overflow of tritium elicited by potassium (K+) and by stimulation of cardiac sympathetic nerve plexus. Prostaglandins E2, I2 and arachidonic acid but not 6-keto-PGF1α reduced K+ and nerve stimulation-induced overflow of tritium. Administration of indomethacin, an inhibitor of cyclooxygenase, increased tritium overflow elicited by either K+ or by nerve stimulation. During infusion of indomethacin, the inhibitory effect of both PGE2 and PGI2 on the K+ or nerve stimulation-induced overflow of tritium remained unaltered. In contrast, the effect of arachidonic acid to reduce K+ or nerve stimulation-induced overflow of tritium was abolished by indomethacin, indicating that the fatty acid inhibits release of tritium by its conversion to a product(s) of cyclooxygenase, presumably PGI2 and PGE2. These data suggest that prostaglandins, particularly PGI2 and PGE2 sythesized in the isolated rat heart act on prejunctional sites to modulate release of the adrenergic transmitter.",
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N2 - In the isolated rat heart perfused with Krebs solution and prelabeled with [3H]noradrenaline, we examined the effect of prostaglandins (PG) I2, E2, 6-keto-PGF1α and their precursor, arachidonic acid, on the overflow of tritium elicited by potassium (K+) and by stimulation of cardiac sympathetic nerve plexus. Prostaglandins E2, I2 and arachidonic acid but not 6-keto-PGF1α reduced K+ and nerve stimulation-induced overflow of tritium. Administration of indomethacin, an inhibitor of cyclooxygenase, increased tritium overflow elicited by either K+ or by nerve stimulation. During infusion of indomethacin, the inhibitory effect of both PGE2 and PGI2 on the K+ or nerve stimulation-induced overflow of tritium remained unaltered. In contrast, the effect of arachidonic acid to reduce K+ or nerve stimulation-induced overflow of tritium was abolished by indomethacin, indicating that the fatty acid inhibits release of tritium by its conversion to a product(s) of cyclooxygenase, presumably PGI2 and PGE2. These data suggest that prostaglandins, particularly PGI2 and PGE2 sythesized in the isolated rat heart act on prejunctional sites to modulate release of the adrenergic transmitter.

AB - In the isolated rat heart perfused with Krebs solution and prelabeled with [3H]noradrenaline, we examined the effect of prostaglandins (PG) I2, E2, 6-keto-PGF1α and their precursor, arachidonic acid, on the overflow of tritium elicited by potassium (K+) and by stimulation of cardiac sympathetic nerve plexus. Prostaglandins E2, I2 and arachidonic acid but not 6-keto-PGF1α reduced K+ and nerve stimulation-induced overflow of tritium. Administration of indomethacin, an inhibitor of cyclooxygenase, increased tritium overflow elicited by either K+ or by nerve stimulation. During infusion of indomethacin, the inhibitory effect of both PGE2 and PGI2 on the K+ or nerve stimulation-induced overflow of tritium remained unaltered. In contrast, the effect of arachidonic acid to reduce K+ or nerve stimulation-induced overflow of tritium was abolished by indomethacin, indicating that the fatty acid inhibits release of tritium by its conversion to a product(s) of cyclooxygenase, presumably PGI2 and PGE2. These data suggest that prostaglandins, particularly PGI2 and PGE2 sythesized in the isolated rat heart act on prejunctional sites to modulate release of the adrenergic transmitter.

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