Regulation of bradykinin-induced cyclic AMP response by quinacrine and prostaglandin E2 and F2? in human synovial fibroblasts

Inflammation ◽  
1979 ◽  
Vol 3 (3) ◽  
pp. 235-242 ◽  
Author(s):  
John V. Fahey ◽  
David S. Newcombe
Keyword(s):  
Cyclic Amp ◽  
Prostaglandin E2 ◽  
Synovial Fibroblasts

scholarly journals Prostaglandin E2 increases cyclic AMP and inhibits endothelin-1 production/secretion by guinea-pig tracheal epithelial cells through EP4 receptors

2001 ◽  
Vol 132 (5) ◽  
pp. 999-1008 ◽  
Author(s):  
Stéphane Pelletier ◽  
Jean Dubé ◽  
Annie Villeneuve ◽  
Fernand Gobeil ◽  
Quan Yang ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Cyclic Amp ◽  
Guinea Pig ◽  
Prostaglandin E2 ◽  
Endothelin 1 ◽  
Tracheal Epithelial Cells ◽  
Tracheal Epithelial

scholarly journals Increase in pituitary adenosine 3′:5′-cyclic monophosphate content and potentiation of growth-hormone release from heifer anterior pituitary slices incubated in the presence of 3-isobutyl-1-methylxanthine

1974 ◽  
Vol 142 (2) ◽  
pp. 295-300 ◽  
Author(s):  
J. George Schofield ◽  
Margaret McPherson
Keyword(s):  
Growth Hormone ◽  
Cyclic Amp ◽  
Prostaglandin E2 ◽  
Anterior Pituitary ◽  
Phosphodiesterase Inhibitor ◽  
Secretory Process ◽  
Hormone Release ◽  
Growth Hormone Release ◽  
Inhibitor Concentration ◽  
Stimulation Of

The release of growth hormone from heifer anterior pituitary slices and the cyclic AMP content of the slices were increased by the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine, both increases being related to inhibitor concentration over the range 0.1–1.0mm. Neither Ba2+(6.9 or 2.3mm), K+(72mm), nor p-chloromercuribenzoate (20μm) had any effect on pituitary cyclic AMP content over a 20min period. 3-Isobutyl-1-methylxanthine potentiated the release of growth hormone in response to Ba2+(2.3mm) and K+(24mm), but the degree of potentiation did not depend on inhibitor concentration in the same way as did tissue cyclic AMP content. 3-Isobutyl-1-methylxanthine decreased the concentration of K+required to give maximum stimulation of growth-hormone release, but did not significantly increase the maximum response to Ba2+. Growth-hormone release in the presence of prostaglandin E2 (1μm) was increased by 3-isobutyl-1-methylxanthine and was inhibited by the prostaglandin antagonist, 7-oxa-13-prostynoic acid, although this antagonist increased the pituitary cyclic AMP concentration and potentiated the prostaglandin E2-induced rise in cyclic AMP content. The stimulation of growth-hormone release by p-chloromercuribenzoate was not potentiated by 3-isobutyl-1-methylxanthine. The data suggest that Ba+and K+act at the same point in the secretory process as 3-isobutyl-1-methylxanthine, although by a different mechanism, and that p-chloromercuribenzoate has a different point of action.

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