Prostaglandins in adrenergic transmission of isolated perfused rat pancreas

M. Hamamdzic, Kafait Malik

Research output: Contribution to journalArticle

20 Citations (Scopus)

Abstract

In the isolated, perfused rat pancreas prostaglandins (PGs) E1 and E2, 1-5 ng/ml, reduced the vasoconstrictor responses to periarterial nerve stimulation and variably affected those to injected norepinephrine. Prostaglandin F2(α) had no consistent effect on the vasoconstrictor responses to both adrenergic stimuli. Stimulation of adrenergic nerves or administration of norepinephrine released a PGE-like substance from the perfused pancreas which was abolished by inhibitors of PG synthesis, acetylsalicyclic acid, indomethacin, meclofenamate, and eicosa-5,8,11,14-tetraynoic acid. The latter 3 agents did not potentiate, but rather reduced the vasoconstrictor responses to both adrenergic stimuli. Arachidonic acid that was converted by the pancreas into PGE2 and PGF2(α) inhibited the vasoconstrictor response to adrenergic stimuli. The latter effect of arachidonic acid was not altered by the simultaneous infusion of PG synthetase inhibitors. Although these results, which could be attributed to a direct effect of inhibitors of PG synthesis and arachidonic acid on adrenergic neuroeffector junction, fail to establish the role of endogenous PGs in modulating adrenergic responses in rat pancreatic vessels, they emphasize the differences in the effect of PGE1 and PGE2 on adrenergic responses in various vascular beds of the rat.

Original languageEnglish (US)
JournalAmerican Journal of Physiology
Volume232
Issue number2
StatePublished - Dec 1 1977
Externally publishedYes

Fingerprint

Adrenergic Agents
Prostaglandins
Pancreas
Vasoconstrictor Agents
Prostaglandin Antagonists
Dinoprostone
Arachidonic Acid
Dinoprost
Alprostadil
Norepinephrine
Neuroeffector Junction
Meclofenamic Acid
Acids
Prostaglandin-Endoperoxide Synthases
Prostaglandins E
Indomethacin
Blood Vessels

All Science Journal Classification (ASJC) codes

  • Physiology (medical)

Cite this

Prostaglandins in adrenergic transmission of isolated perfused rat pancreas. / Hamamdzic, M.; Malik, Kafait.

In: American Journal of Physiology, Vol. 232, No. 2, 01.12.1977.

Research output: Contribution to journalArticle

@article{277899d2beb04b8396c3f0fa10466f35,
title = "Prostaglandins in adrenergic transmission of isolated perfused rat pancreas",
abstract = "In the isolated, perfused rat pancreas prostaglandins (PGs) E1 and E2, 1-5 ng/ml, reduced the vasoconstrictor responses to periarterial nerve stimulation and variably affected those to injected norepinephrine. Prostaglandin F2(α) had no consistent effect on the vasoconstrictor responses to both adrenergic stimuli. Stimulation of adrenergic nerves or administration of norepinephrine released a PGE-like substance from the perfused pancreas which was abolished by inhibitors of PG synthesis, acetylsalicyclic acid, indomethacin, meclofenamate, and eicosa-5,8,11,14-tetraynoic acid. The latter 3 agents did not potentiate, but rather reduced the vasoconstrictor responses to both adrenergic stimuli. Arachidonic acid that was converted by the pancreas into PGE2 and PGF2(α) inhibited the vasoconstrictor response to adrenergic stimuli. The latter effect of arachidonic acid was not altered by the simultaneous infusion of PG synthetase inhibitors. Although these results, which could be attributed to a direct effect of inhibitors of PG synthesis and arachidonic acid on adrenergic neuroeffector junction, fail to establish the role of endogenous PGs in modulating adrenergic responses in rat pancreatic vessels, they emphasize the differences in the effect of PGE1 and PGE2 on adrenergic responses in various vascular beds of the rat.",
author = "M. Hamamdzic and Kafait Malik",
year = "1977",
month = "12",
day = "1",
language = "English (US)",
volume = "232",
journal = "AM.J.PHYSIOL.",
issn = "0002-9513",
publisher = "American Physiological Society",
number = "2",

}

TY - JOUR

T1 - Prostaglandins in adrenergic transmission of isolated perfused rat pancreas

AU - Hamamdzic, M.

AU - Malik, Kafait

PY - 1977/12/1

Y1 - 1977/12/1

N2 - In the isolated, perfused rat pancreas prostaglandins (PGs) E1 and E2, 1-5 ng/ml, reduced the vasoconstrictor responses to periarterial nerve stimulation and variably affected those to injected norepinephrine. Prostaglandin F2(α) had no consistent effect on the vasoconstrictor responses to both adrenergic stimuli. Stimulation of adrenergic nerves or administration of norepinephrine released a PGE-like substance from the perfused pancreas which was abolished by inhibitors of PG synthesis, acetylsalicyclic acid, indomethacin, meclofenamate, and eicosa-5,8,11,14-tetraynoic acid. The latter 3 agents did not potentiate, but rather reduced the vasoconstrictor responses to both adrenergic stimuli. Arachidonic acid that was converted by the pancreas into PGE2 and PGF2(α) inhibited the vasoconstrictor response to adrenergic stimuli. The latter effect of arachidonic acid was not altered by the simultaneous infusion of PG synthetase inhibitors. Although these results, which could be attributed to a direct effect of inhibitors of PG synthesis and arachidonic acid on adrenergic neuroeffector junction, fail to establish the role of endogenous PGs in modulating adrenergic responses in rat pancreatic vessels, they emphasize the differences in the effect of PGE1 and PGE2 on adrenergic responses in various vascular beds of the rat.

AB - In the isolated, perfused rat pancreas prostaglandins (PGs) E1 and E2, 1-5 ng/ml, reduced the vasoconstrictor responses to periarterial nerve stimulation and variably affected those to injected norepinephrine. Prostaglandin F2(α) had no consistent effect on the vasoconstrictor responses to both adrenergic stimuli. Stimulation of adrenergic nerves or administration of norepinephrine released a PGE-like substance from the perfused pancreas which was abolished by inhibitors of PG synthesis, acetylsalicyclic acid, indomethacin, meclofenamate, and eicosa-5,8,11,14-tetraynoic acid. The latter 3 agents did not potentiate, but rather reduced the vasoconstrictor responses to both adrenergic stimuli. Arachidonic acid that was converted by the pancreas into PGE2 and PGF2(α) inhibited the vasoconstrictor response to adrenergic stimuli. The latter effect of arachidonic acid was not altered by the simultaneous infusion of PG synthetase inhibitors. Although these results, which could be attributed to a direct effect of inhibitors of PG synthesis and arachidonic acid on adrenergic neuroeffector junction, fail to establish the role of endogenous PGs in modulating adrenergic responses in rat pancreatic vessels, they emphasize the differences in the effect of PGE1 and PGE2 on adrenergic responses in various vascular beds of the rat.

UR - http://www.scopus.com/inward/record.url?scp=0017595367&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0017595367&partnerID=8YFLogxK

M3 - Article

C2 - 190895

AN - SCOPUS:0017595367

VL - 232

JO - AM.J.PHYSIOL.

JF - AM.J.PHYSIOL.

SN - 0002-9513

IS - 2

ER -