Direct effect of adenosine on prolactin secretion at the level of the single rat lactotroph: involvement of pertussis toxin-sensitive and -insensitive transducing mechanisms

in Journal of Molecular Endocrinology
Authors:
A Scorziello
Search for other papers by A Scorziello in
Current site
Google Scholar
PubMed
Close
,
E Landolfi
Search for other papers by E Landolfi in
Current site
Google Scholar
PubMed
Close
,
M Grimaldi
Search for other papers by M Grimaldi in
Current site
Google Scholar
PubMed
Close
,
O Meucci
Search for other papers by O Meucci in
Current site
Google Scholar
PubMed
Close
,
C Ventra
Search for other papers by C Ventra in
Current site
Google Scholar
PubMed
Close
,
A Avallone
Search for other papers by A Avallone in
Current site
Google Scholar
PubMed
Close
,
A Postiglione
Search for other papers by A Postiglione in
Current site
Google Scholar
PubMed
Close
, and
G Schettini
Search for other papers by G Schettini in
Current site
Google Scholar
PubMed
Close
View More View Less
Restricted access

USD  $0.01
USD  $0.01

USD  $0.01
USD  $0.01

USD  $0.01
USD  $0.01

USD  $0.01
USD  $0.01

USD  $0.01
USD  $0.01

USD  $0.01
USD  $0.01

USD  $0.01
USD  $0.01

USD  $0.01
USD  $0.01

USD  $0.01
USD  $0.01

USD  $1.00
USD  $1.00

USD  $1.00
USD  $1.00

USD  $1.00
USD  $1.00

ABSTRACT

We studied the effect of adenosine on prolactin secretion by the anterior pituitary, and the transduction mechanisms whereby the purine exerts its action. Adenosine inhibited prolactin release in basal and in vasoactive intestinal peptide (VIP)- or TRH-stimulated conditions. Pertussis toxin pretreatment reduced the inhibition of VIP-stimulated prolactin secretion which was induced by adenosine, while it completely abolished the effect of the purine on TRH-evoked prolactin release. In membrane preparations of anterior pituitary cells, adenosine reduced the adenylate cyclase activity stimulated by VIP. Such an inhibition was not blocked by pertussis toxin pretreatment.

Furthermore, the purine reduced TRH-stimulated inositol phosphate production in cultured anterior pituitary cells, an effect that was reversed by pretreatment with pertussis toxin. In addition, the nucleoside did not significantly affect the TRH-induced rise in intracellular calcium.

In conclusion, our data show that adenosine inhibits prolactin secretion, acting on purinergic receptors coupled to the adenylate cyclase enzyme and phospholipase C. The effect of the nucleoside on adenylate cyclase seems to be achieved either by the involvement of an adenosine receptor coupled to the catalytic subunit of the enzyme via a pertussis toxin-sensitive G protein, or by the activation of a site directly coupled to the catalytic subunit of the adenylate cyclase (the P site). Its effect on phospholipase C seems to be mediated by a purinergic receptor coupled to the intracellular effector via a pertussis toxin-sensitive G protein.