5-HT-stimulated arachidonic acid release from labeled phosphatidylinositol in blowfly salivary glands

I. Litosch, Y. Saito, J. N. Fain

Research output: Contribution to journalArticle

Abstract

In blowfly salivary glands, breakdown of phosphatidylinositol has been linked to the activation of hormone-sensitive Ca2+ channels. Addition of 5-hydroxytryptamine to blowfly salivary glands stimulated the breakdown of phosphatidylinositol prelabeled with 32P or [3H]arachidonic acid. This was associated with a transient accumulation of [3H]arachidonic-labeled diglyceride. There was no appreciable effect of 5-hydroxytryptamine on breakdown of phosphatidylethanolamine or phosphatidylcholine labeled with 32P or [3H]arachidonic acid, indicating that phosphatidylinositol was the immediate source of diglyceride. Extracellular Ca2+ was necessary for [3H]arachidonic acid but not 32P loss from phosphatidylinositol. Addition of arachidonic acid to salivary glands did not stimulate salivary gland secretion or 45Ca flux. In contrast, 5-hydroxytryptamine stimulated both salivary gland secretion and 45Ca flux. These results indicate that, although [3H]arachidonic acid is incorporated into phosphatidylinositol and its release from this phospholipid is increased by 5-hydroxytryptamine, the liberated arachidonic acid does not stimulate salivery gland secretion or 45Ca flux.

Original languageEnglish
JournalAmerican Journal of Physiology - Cell Physiology
Volume12
Issue number3
StatePublished - Dec 1 1982
Externally publishedYes

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Phosphatidylinositols
Salivary Glands
Arachidonic Acid
Serotonin
Diglycerides
Fluxes
Phosphatidylcholines
Phospholipids
Chemical activation
Hormones

ASJC Scopus subject areas

  • Cell Biology
  • Clinical Biochemistry
  • Physiology

Cite this

5-HT-stimulated arachidonic acid release from labeled phosphatidylinositol in blowfly salivary glands. / Litosch, I.; Saito, Y.; Fain, J. N.

In: American Journal of Physiology - Cell Physiology, Vol. 12, No. 3, 01.12.1982.

Research output: Contribution to journalArticle

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