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

1982 ◽  
Vol 243 (5) ◽  
pp. C222-C226 ◽  
Author(s):  
I. Litosch ◽  
Y. Saito ◽  
J. N. Fain
Keyword(s):  
Arachidonic Acid ◽  
Salivary Gland ◽  
Salivary Glands ◽  
Gland Secretion ◽  
Appreciable Effect ◽  
Arachidonic Acid Release ◽  
Salivary Gland Secretion ◽  
Hormone Sensitive ◽  
Acid Release ◽  
Ca2 Channels

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 salivary gland secretion or 45Ca flux.

scholarly journals Forskolin as an activator of cyclic AMP accumulation and secretion in blowfly salivary glands

1982 ◽  
Vol 204 (1) ◽  
pp. 147-151 ◽  
Author(s):  
I Litosch ◽  
Y Saito ◽  
J N Fain
Keyword(s):  
Salivary Gland ◽  
Cyclic Amp ◽  
Adenylate Cyclase ◽  
Salivary Glands ◽  
Mammalian Cells ◽  
Salivary Secretion ◽  
Gland Secretion ◽  
Cyclic Amp Accumulation ◽  
Salivary Gland Secretion ◽  
Stimulation Of

Forskolin is a diterpene that activates adenylate cyclase in a variety of mammalian cells. In addition of forskolin to blowfly salivary glands increased cyclic AMP accumulation and salivary secretion. There was a small increase in transepithelial movement of labelled Ca2+. Forskolin did not induce breakdown of labelled phosphatidylinositol or inhibit the stimulation of phosphatidylinositol breakdown caused by 5-hydroxytryptamine. These data indicate that forskolin can mimic all the effects of 5-hydroxytryptamine on salivary-gland secretion that have been attributed to cyclic AMP.

The foregut glands of vermivorous cone shells

1971 ◽  
Vol 19 (4) ◽  
pp. 313 ◽  
Author(s):  
H Marsh
Keyword(s):  
Salivary Gland ◽  
Salivary Glands ◽  
Protease Activity ◽  
Proteolytic Enzymes ◽  
Gland Secretion ◽  
Salivary Gland Secretion ◽  
Acid Mucosubstances

Salivary, snout, and secondary salivary glands are recorded in the foregut region of Conus Javidus, C. lividus, C. litteratus, C. miles, C. vexillum, and C. virgo. C. imperialis has a salivary gland only. The histology and histochemistry of these glands in C. Javidus and C, lividus is investigated. The salivary gland secretion consists of granules composed of polysaccharide and protein. The snout gland secretes sulphated acid mucosubstances. The secondary salivary gland secretion contains polysaccharide and protein. Protease activity was detected histochemically in the salivary gland, indicating that a function of this gland in Conus is the secretion of proteolytic enzymes into the short arm of the radular sac. The functions of the snout gland, which is peculiar to some species of Conus, and of the secondary salivary gland, which occurs sporadically throughout the Stenoglossidae, are not immediately apparent.

Characterization of Ca2+ Channels and G Proteins Involved in Arachidonic Acid Release by Endothelin-1/EndothelinA Receptor

2003 ◽  
Vol 64 (3) ◽  
pp. 689-695 ◽  
Author(s):  
Yoshifumi Kawanabe ◽  
Kazuhiko Nozaki ◽  
Nobuo Hashimoto ◽  
Tomoh Masaki
Keyword(s):  
Arachidonic Acid ◽  
G Proteins ◽  
Arachidonic Acid Release ◽  
Endothelin 1 ◽  
Acid Release ◽  
Ca2 Channels

PGE2 release by bradykinin in human airway smooth muscle cells: involvement of cyclooxygenase-2 induction

1997 ◽  
Vol 273 (6) ◽  
pp. L1132-L1140 ◽  
Author(s):  
Linhua Pang ◽  
Alan J. Knox
Keyword(s):  
Arachidonic Acid ◽  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Arachidonic Acid Release ◽  
Human Airway Smooth Muscle ◽  
Short Term ◽  
Human Airway ◽  
Acid Release ◽  
Cox 2

Prostanoids may be involved in bradykinin (BK)-induced bronchoconstriction in asthma. We investigated whether cyclooxygenase (COX)-2 induction was involved in prostaglandin (PG) E2 release by BK in cultured human airway smooth muscle (ASM) cells and analyzed the BK receptor subtypes responsible. BK stimulated PGE2release, COX activity, and COX-2 induction in a concentration- and time-dependent manner. It also time dependently enhanced arachidonic acid release. In short-term (15-min) experiments, BK stimulated PGE2 generation but did not increase COX activity or induce COX-2. In long-term (4-h) experiments, BK enhanced PGE2 release and COX activity and induced COX-2. The long-term responses were inhibited by the protein synthesis inhibitors cycloheximide and actinomycin D and the steroid dexamethasone. The effects of BK were mimicked by the B2-receptor agonist [Tyr(Me)8]BK, whereas the B1 agonist des-Arg9-BK was weakly effective at high concentrations. The B2antagonist HOE-140 potently inhibited all the effects, but the B1 antagonist des-Arg9,(Leu8)-BK was inactive. This study is the first to demonstrate that BK can induce COX-2. Conversion of increased arachidonic acid release to PGE2 by COX-1 is mainly involved in the short-term effect, whereas B2 receptor-related COX-2 induction is important in the long-term PGE2 release.

Sign in / Sign up

Export Citation Format

Share Document