Cyclic 3’,5’-Adenosine Monophosphate Mediates Dopamine D1-Stimulated Growth Hormone Release from Goldfish Pituitary Cells

1994 ◽  
Vol 60 (4) ◽  
pp. 410-417 ◽  
Author(s):  
Anderson On-Lam Wong ◽  
Glen van der Kraak ◽  
John Philip Chang
1969 ◽  
Vol 25 (7) ◽  
pp. 750-751 ◽  
Author(s):  
E. E. Müller ◽  
A. Pecile ◽  
M. Kabir Naimzada ◽  
Gabriella Ferrario

1989 ◽  
Vol 67 (10) ◽  
pp. 1321-1325
Author(s):  
M. S. Sheppard ◽  
B. A. Eatock ◽  
R. M. Bala

We have shown in the companion paper that somatotrophs dispersed from streptozotocin diabetic rats exhibit altered sensitivity to the natural hypothalamic controlling hormones, growth hormone releasing factor and somatostatin. We have further studied the effects on growth hormone release from dispersed adenohypophysial cells of normal and streptozotocin diabetic rats of stimulation by compounds that increase cyclic 3′,5′-adenosine monophosphate formation or inhibit its breakdown and of a phorbol ester. The cells of the diabetic rats had no change in sensitivity in response to either cholera toxin or forskolin. A phosphodiesterase inhibitor caused an equal GH release from cells of both diabetic and normal animals after 60 min of incubation. There was no change in sensitivity of the cells of diabetic animals or in the maximal reponse of these cells to the phorbol ester 12-O-tetradecanoylphorbol 13-acetate when compared with normal cells. A low calcium medium that blocked growth hormone releasing factor stimulated growth hormone release from normal rat cells also blocked it from the cells of the diabetic rats. These results suggest that the defect in response of the somatotrophs of diabetic animals is specific and only occurs with the hypothalamic hormones and not with other secretagogues.Key words: growth hormone, diabetes, streptozotocin, cyclic AMP, phorbol ester.


1998 ◽  
Vol 68 (3) ◽  
pp. 192-200 ◽  
Author(s):  
Christa L. Fry ◽  
David R. Gunter ◽  
Christopher D. McMahon ◽  
Barbara Steele ◽  
James L. Sartin

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