Pharmacological characterization of the angiotensin receptor negatively coupled with adenylate cyclase in rat anterior pituitary gland

Details

Serval ID
serval:BIB_B11305A8389E
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Pharmacological characterization of the angiotensin receptor negatively coupled with adenylate cyclase in rat anterior pituitary gland
Journal
Endocrinology
Author(s)
Marie  J., Gaillard  R. C., Schoenenberg  P., Jard  S., Bockaert  J.
ISSN
0013-7227 (Print)
Publication state
Published
Issued date
03/1985
Volume
116
Number
3
Pages
1044-50
Notes
Comparative Study
Journal Article
Research Support, Non-U.S. Gov't --- Old month value: Mar
Abstract
Angiotensin II (AII) inhibited anterior pituitary adenylate cyclase. Whereas GTP was necessary to fully express the AII inhibitory effect, Na+ was not required. The magnitude of inhibition (42 +/- 6%) permitted a pharmacological characterization of the AII receptor involved in adenylate cyclase inhibition. Angiotensin I (AI) was less potent than AII, and deletion of aminoacids in the N-terminal position resulted in a progressive reduction of the Ki (peptide concentration producing half-maximal inhibition). The Ki values were 3 +/- 0.9, 10, and 700 nM for AII, angiotensin III (AIII), and des-Asp, des-Arg-AII, respectively. Sarcosine in position 1 [( Sar, Phe]AII) increased the potency of inhibition (Ki = 0.12 +/- 0.12 nM). Different antagonists of the AII receptors appeared to be partial agonists. There was a very close correlation (r = 0.98) between the respective potencies of a series of AII analogs to inhibit adenylate cyclase and the potencies of these analogs to elicit PRL or ACTH release or to bind to AII-binding sites. Dopamine and AII inhibition of anterior pituitary adenylate cyclase were not additive. This suggests that both receptors are on the same cell and likely on lactotrophs. This hypothesis agrees with the observation that vasoactive intestinal peptide stimulation of adenylate cyclase was inhibited by AII, whereas corticotropin-releasing factor stimulation was unaffected. Although dopamine and AII inhibited the same adenylate cyclase, they had opposing effects on PRL release (inhibition and stimulation, respectively). The possible significance of this observation is related to a model implying that PRL release can be elicited through either a Ca+2 or a cAMP pathway.
Keywords
Adenylate Cyclase/antagonists & inhibitors/*metabolism Angiotensin II/pharmacology Animals Chemistry Corticotropin-Releasing Hormone/pharmacology Dopamine/pharmacology Drug Interactions Female Guanosine Triphosphate/pharmacology Pituitary Gland, Anterior/*metabolism Rats Rats, Inbred Strains Receptors, Angiotensin/*metabolism Receptors, Cell Surface/*metabolism Sodium/pharmacology Structure-Activity Relationship Vasoactive Intestinal Peptide/pharmacology
Pubmed
Web of science
Create date
15/02/2008 16:58
Last modification date
20/08/2019 15:20
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