Effects of prolactin on aldosterone secretion in rat zona glomerulosa cells

Acute effects and action mechanisms of prolactin (PRL) on aldosterone secretion in zona glomerulosa (ZG) cells were investigated in ovariectomized rats. Administration of ovine PRL (oPRL) increased aldosterone secretion in a dose‐dependent manner. Incubation of [3H]‐pregnenolone combined with oPRL i...

Full description

Saved in:
Bibliographic Details
Published inJournal of cellular biochemistry Vol. 72; no. 2; pp. 286 - 293
Main Authors Kau, Mei-Mei, Lo, Ming-Jae, Tsai, Shiow-Chwen, Chen, Jiann-Jong, Pu, Hsiao-Fung, Chien, Eileen Jea, Chang, Ling-Ling, Wang, Paulus S.
Format Journal Article
LanguageEnglish
Published New York John Wiley & Sons, Inc 01.02.1999
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Acute effects and action mechanisms of prolactin (PRL) on aldosterone secretion in zona glomerulosa (ZG) cells were investigated in ovariectomized rats. Administration of ovine PRL (oPRL) increased aldosterone secretion in a dose‐dependent manner. Incubation of [3H]‐pregnenolone combined with oPRL increased the production of [3H]‐aldosterone and [3H]‐deoxycorticosterone but decreased the accumulation of [3H]‐corticosterone. Administration of oPRL produced a marked increase of adenosine 3′,5′‐cyclic monophosphate (cAMP) accumulation in ZG cells. The stimulatory effect of oPRL on aldosterone secretion was attenuated by the administration of angiotensin II (Ang II) and high potassium. The Ca2+ chelator, ethylene glycol‐bis(β‐aminoethyl ether)‐N,N,N′,N′‐tetraacetic acid (EGTA, 10−2 M), inhibited the basal release of aldosterone and completely suppressed the stimulatory effects of oPRL on aldosterone secretion. The stimulatory effects of oPRL on aldosterone secretion were attenuated by the administration of nifedipine (L‐type Ca2+ channel blocker) and tetrandrine (T‐type Ca2+ channel blocker). These data suggest that the increase of aldosterone secretion by oPRL is in part due to (1) the increase of cAMP production, (2) the activation of both L‐ and T‐type Ca2+ channels, and (3) the activation of 21‐hydroxylase and aldosterone synthase in rat ZG cells. J. Cell. Biochem. 72:286–293, 1999. © 1999 Wiley‐Liss, Inc.
Bibliography:VGH-NYMU Joint Research Program - No. VGHYM 87-S4-27
Medical Research and Advancement Foundation
ArticleID:JCB13
Tsou's Foundation, ROC
ark:/67375/WNG-F8G7BNR5-V
istex:3543BA88F3C1B455686C969C9D051F79911C4264
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0730-2312
1097-4644
DOI:10.1002/(SICI)1097-4644(19990201)72:2<286::AID-JCB13>3.0.CO;2-4