Influence of in vivo Reproductive Endocrine State on Growth Hormone-Releasing Factor Stimulated Adenylate Cyclase Activity in Anterior Pituitary Fragments

1993 ◽  
Vol 57 (1) ◽  
pp. 63-69
Author(s):  
Steven M. Gabriel ◽  
Edward H. Hunnicut ◽  
William J. Millard ◽  
Thomas M. Badger ◽  
James A. Nathanson
Endocrinology ◽  
1981 ◽  
Vol 109 (3) ◽  
pp. 990-992 ◽  
Author(s):  
PAULA LEPPERT ◽  
V. JAMES GUILLORY ◽  
LIBBIE J. RUSSO ◽  
WAYNE V. MOORE

1979 ◽  
Vol 178 (1) ◽  
pp. 217-221 ◽  
Author(s):  
M D Houslay ◽  
R W Palmer

1. Synthetic lysophosphatidylcholines inhibit the glucagon-stimulated adenylate cyclase activity of rat liver plasma membranes at concentrations two to five times lower than those needed to inhibit the fluoride-stimulated activity. 2. Specific 125I-labelled glucagon binding to hormone receptors is inhibited at concentrations similar to those inhibiting the fluoride-stimulated activity. 3. At concentrations of lysophosphatidylcholines immediately below those causing inhibition, an activation of adenylate cyclase activity or hormone binding was observed. 4 These effects are essentially reversible. 5. We conclude that the increased sensitivity of glucagon-stimulated adenylate cyclase to inhibition may be due to the lysophosphatidylcholines interfering with the physical coupling between the hormone receptor and catalytic unit of adenylate cyclase. 6. We suggest that, in vivo, it is possible that lysophosphatidylcholines may modulate the activity of adenylate cyclase only when it is in the hormone-stimulated state.


1990 ◽  
Vol 5 (1) ◽  
pp. 69-76 ◽  
Author(s):  
G. Schettini ◽  
E. Landolfi ◽  
O. Meucci ◽  
T. Florio ◽  
M. Grimaldi ◽  
...  

ABSTRACT The effect of adenosine and its analogue ( − )-N6-R-phenylisopropyladenosine (PIA) on both anterior pituitary adenylate cyclase activity and prolactin secretion was examined in the rat. Adenosine inhibited basal adenylate cyclase activity in a dose-dependent manner and also reduced the stimulation of the enzyme by vasoactive intestinal peptide (VIP). Likewise, in primary cultures of anterior pituitary cells, adenosine decreased prolactin secretion in both basal and VIP-stimulated conditions. In perifusion experiments, adenosine also inhibited prolactin release in both basal and TRH-stimulated conditions. PIA produced a biphasic pattern of response of basal adenylate cyclase activity, being inhibitory at low and stimulatory at high concentrations. In VIP-stimulated conditions, low concentrations of PIA inhibited both adenylate cyclase activity and prolactin release from primary cultures of pituitary cells, while no additive stimulatory effect was seen at high concentrations. Similarly, low concentrations of PIA reduced both basal and TRH-stimulated prolactin release from perifused pituitaries, while increasing PIA concentrations restored prolactin release. These data show that adenosine affects basal and stimulated prolactin secretion from anterior pituitary cells. Adenosine receptors seem to be coupled to the adenylate cyclase system in the anterior pituitary gland, suggesting a possible relationship between the effect of adenosine on adenylate cyclase activity and prolactin secretion.


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