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Adenosine A1 receptors inhibit both adenylate cyclase activity and TRH-activated Ca2+ channels by a pertussis toxin-sensitive mechanism in GH3 cells.

Abstract：

:The present study has examined the effects of adenosine A1 receptors on second messenger processes in GH3 cells. A1 receptors are present which are shown to inhibit adenylate cyclase in a GTP-requiring manner. Hormone (VIP) stimulation is also absolutely required for the observation of inhibition. Adenosine A1 receptor analogues also inhibit TRH-stimulated [Ca2+]i-mobilization in GH3 cells. Both effects of the adenosine receptor agonists are apparently mediated by pertussis toxin substrates, of which there are two--41,000 and 40,000 daltons respectively--in these cells. Somatostatin exerts analogous effects to the adenosine agonists in GH3 cells. Thus it may turn out that a general property of 'cyclase inhibitory receptors' is also to inhibit [Ca2+]i-mobilization in the same cells, when such mechanisms are present.

journal_name

Cell Signal

journal_title

Cellular signalling

authors

Cooper DM,Caldwell KK,Boyajian CL,Petcoff DW,Schlegel W

doi

10.1016/0898-6568(89)90023-5

subject

Has Abstract

pub_date

1989-01-01 00:00:00

pages

85-97

issue

1

eissn

0898-6568

issn

1873-3913

pii

0898-6568(89)90023-5

journal_volume

1

pub_type

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