AJP - Endocrinology and Metabolism, Vol 267, Issue 6 E842-E846, Copyright © 1994 by American Physiological Society
Endothelin-1 modulates renin and prolactin release from human decidua by different mechanisms
H. S. Chao, A. M. Poisner, R. Poisner and S. Handwerger
Department of Pediatrics and the Perinatal Research Center, Children's Hospital Medical Center, University of Cincinnati, Ohio 45229.
Endothelin (ET)-1 stimulates the synthesis and release of renin and
inhibits the expression of prolactin (PRL) from term human decidual cells.
To examine the mechanisms by which ET-1 exerts its differential effects on
renin and PRL expression, we have studied total renin and PRL release from
term human decidual cells in response to pharmacological agents that affect
calcium- and protein kinase C-dependent mechanisms. Calcium ionophore
A-23187 stimulated basal renin release and potentiated ET-1-stimulated
renin release but had no effect on basal or ET-inhibited PRL release. The
calcium channel blocker nifedipine inhibited ET-1-stimulated renin release
but had no effect on PRL release. The protein kinase C agonist phorbol
12-myristate 13-acetate (PMA) stimulated basal renin release and
potentiated the effect of ET-1 on renin release. However, PMA inhibited
basal PRL release and also enhanced the inhibitory effect of ET-1. The PKC
inhibitor staurosporine increased basal PRL release and completely reversed
the inhibitory effect of ET on PRL release. These results indicate that the
effects of ET-1 on both decidual renin and PRL release are dependent on the
activation of protein kinase C. However, the effect of ET-1 on renin
release appears to be dependent on extracellular calcium, whereas the
effect on PRL is not influenced by extracellular calcium.
