AJP - Endocrinology and Metabolism, Vol 254, Issue 4 E476-E481, Copyright © 1988 by American Physiological Society
Inhibition by extracellular Na+ replacement of GRF-induced GH secretion from rat pituitary cells
M. Kato, M. A. Hattori and M. Suzuki
Department of Physiology, Gunma University, Maebashi, Japan.
To further clarify the ionic mechanism of the action of growth hormone
(GH)-releasing factor (hGRF) on GH secretion, the involvement of
extracellular Na+ was studied in perifused dispersed rat anterior pituitary
cells. Replacing extracellular Na+ with mannitol or
tris(hydroxymethyl)aminomethane (Tris+) suppressed hGRF- and dibutyryl
adenosine 3',5'-cyclic monophosphate (DBcAMP)-induced GH secretion. The
peak responses to a 2-min application of 1 nM hGRF were 165.0 +/- 5.6 ng/ml
(normal medium, mean +/- SE), 21.2 +/- 1.4 ng/ml (Na+-free, mannitol
medium), and 18.0 +/- 1.7 ng/ml (Na+-free, Tris+ medium). GH secretion
induced by DBcAMP was also suppressed by Na+ replacement to less than 50%
of that in normal medium. However, either 15 or 30 mM KCl-stimulated GH
secretion was not markedly affected by replacement of Na+ with either
compound. Tetrodotoxin, a voltage-sensitive Na+ channel blocker, had no
effect on either hGRF- or excess K+-induced GH secretion. cAMP production
by hGRF was not greatly affected by replacing extracellular Na+. Thus
extracellular Na+ plays an important role in hGRF-induced GH secretion,
especially in the process after cAMP production. The involvement of
cAMP-sensitive Na+ channels in hGRF-stimulated GH secretion is discussed.
