Efonidipine can block both L- and T- type Ca2+ channels. In a previous in vitro study, we clarified that
efonidipine dramatically suppresses
aldosterone secretion from human adrenocortical
tumor cells during
angiotensin II (Ang II)- and K+-stimulation, whereas
nifedipine, a dominant L-type Ca2+ channel antagonist, does not. This study was conducted to assess the in vivo effects of
efonidipine and
nilvadipine on the plasma
aldosterone concentration. Placebo, 40 mg of
efonidipine, or 2 mg of
nilvadipine was administered to five healthy male volunteers. Hemodynamic parameters (pulse rate [PR] and blood pressure [BP]), plasma concentrations of neurohormonal factors (plasma
renin activity, Ang II,
aldosterone, and
adrenocorticotropic hormone [
ACTH]), and serum concentrations of Na+ and K+ were measured before and 6 h after administration of the agents. All three agents had little effect on PR and BP.
Efonidipine and
nilvadipine significantly increased plasma
renin activity and Ang II. Both had little effect on
ACTH, Na+, and K+. The plasma
aldosterone concentration was significantly decreased after
efonidipine treatment (88.3 +/- 21.3 to 81.6 +/- 24.9 pg/ml, p = 0.0407), whereas it was significantly increased after
nilvadipine treatment (66.5 +/- 12.2 to 82.17 +/- 16.6 pg/ml, p = 0.0049). Placebo had little effect on neurohormonal factors.
Efonidipine decreased plasma
aldosterone concentration despite the increase in plasma
renin activity and Ang II, suggesting that T-type Ca2+ channels may also play an essential role in the secretion of
aldosterone in healthy human volunteers.