Effects of phosphatidic acid on islet cell phosphoinositide hydrolysis, Ca2+, and adenylate cyclase

Diabetes ◽  
1989 ◽  
Vol 38 (9) ◽  
pp. 1187-1192 ◽  
Author(s):  
M. E. Dunlop ◽  
R. G. Larkins
Keyword(s):  
Adenylate Cyclase ◽  
Phosphatidic Acid ◽  
Islet Cell ◽  
Phosphoinositide Hydrolysis

Cloned rat M3 muscarinic receptors mediate phosphoinositide hydrolysis but not adenylate cyclase inhibition

FEBS Letters ◽  
1988 ◽  
Vol 239 (2) ◽  
pp. 174-178 ◽  
Author(s):  
Ronit Pinkas-Kramarski ◽  
Reuven Stein ◽  
Yitzhak Zimmer ◽  
Mordechai Sokolovsky
Keyword(s):  
Adenylate Cyclase ◽  
Muscarinic Receptors ◽  
Phosphoinositide Hydrolysis ◽  
Adenylate Cyclase Inhibition

scholarly journals Cyclic AMP does not inhibit collagen-induced platelet signal transduction

1992 ◽  
Vol 283 (3) ◽  
pp. 889-892 ◽  
Author(s):  
J B Smith ◽  
C Dangelmaier ◽  
M A Selak ◽  
B Ashby ◽  
J Daniel
Keyword(s):  
Signal Transduction ◽  
Platelet Aggregation ◽  
Cyclic Amp ◽  
Adenylate Cyclase ◽  
Phosphatidic Acid ◽  
Platelet Adhesion ◽  
Thromboxane A2 ◽  
Prostaglandin I2 ◽  
Primary Event ◽  
Adhesion Of Platelets

The adhesion of platelets to collagen and their activation is the primary event in haemostasis. Following adhesion, platelet aggregation mediated by ADP, thromboxane A2 and thrombin leads to the formation of a platelet plug. It is known that platelet activation by each of these agonists involves an increase in the cytosolic free Ca2+ concentration, and this has been thought to be controlled by cyclic AMP. However, we report here that while signal transduction induced by ADP plus a thromboxane mimetic (U46619), or by thrombin, is inhibited by stimulators of adenylate cyclase such as a prostaglandin I2 (PGI2) analogue (Iloprost), PGD2 and forskolin, elevation of cyclic AMP does not inhibit either platelet adhesion to collagen or the associated Ca2+ mobilization, phosphatidic acid formation or 5-hydroxytryptamine secretion. Furthermore, collagen did not lower elevated levels of cyclic AMP in platelets measured in the presence of both a thromboxane antagonist and an ADP-removing system. The present results are discussed in the context of previous findings.

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