The effect of osmotic changes on aldosterone production, [Ca2+](i) and volt
age-gated Ca2+ currents, was studied in cultured rat glomerulosa cells. Alt
eration of osmolarity by sucrose addition in the 250-330 mosM range did not
influence aldosterone production per se, but it substantially affected K+-
stimulated aldosterone production. Hyposmosis markedly increased the hormon
e response evoked by raising [K+] from 3.6 to 5 mM, whereas hyperosmosis ha
d a mild decreasing effect. Cytoplasmic [Ca2+](i), measured in single glome
rulosa cells, did not show detectable change in response to either hyposmot
ic or hyperosmotic exposure, but the [Ca2+](i) signal evoked by elevation o
f [K+] to 5 mM was augmented in hyposmotic solution. The osmosensitivity of
the transient (T)-type and long-lasting (L)-type voltage-gated Ca2+ curren
ts was studied using the nystatin-perforated voltage-clamp technique. Lower
ing osmolarity to 250 mosM significantly increased the amplitude of the T-t
ype current, and it had a transient augmenting effect on L-type current amp
litude. Hyperosmotic solution (330 mosh) reduced L-type current amplitude b
ut did not evoke significant change in T-type current. These results indica
te that the responsiveness of rat glomerulosa cells to physiological elevat
ion of [K+] is remarkably influenced by changes in osmolarity by means of m
odulating the function of voltage-gated Ca2+ channels.