The effect of [Asu1,7]-eel calcitonin (ECT), which is an equipotent analog of eel calcitonin (CT), on GH secretion was investigated in freely moving conscious male rats. Pulsatile GH secretion was completely inhibited by iv injection of ECT (2.5 micrograms/rat). The mean 6-h plasma GH levels, 9.54 +/- 2.34 ng/ml (mean +/- SEM) in ECT-treated rats, were significantly lower than those in saline-treated rats (69.9 +/- 9.4 ng/ml, P less than 0.001). In order to examine the action of ECT on the central nervous system, 25 ng ECT dissolved in 10 microliters saline were injected into the lateral ventricle of conscious male rats. The bursts of GH secretion were completely abolished by this dose of intraventricularly (ivt) injected ECT. The mean 6-h GH levels 5.8 +/- 0.8 ng/ml, were also significantly lower than those in control rats (35.8 +/- 6.6 ng/ml, P less than 0.01). Serum Ca levels did not change after the ivt injection of 25 ng ECT but fell significantly after the iv injection of 2.5 micrograms ECT. In order to clarify the inhibitory mechanism of GH secretion by ECT, the effect of ECT on the release of GH elicited by prostaglandin E1 (PGE1), a well-known GH secretagogue acting directly on the pituitary, was examined in vivo as well as in vitro. Both ivt (2.5, 25, or 250 ng/10 microliters X rat) and iv (2.5 or 25 micrograms/rat) injections of ECT caused a significant and dose-dependent suppression of PGE1-induced GH rises in conscious rats. In contrast, 10(-8) to 10(-7) M ECT failed to affect the baseline secretion of GH and its release by 5 X 10(-6) M PGE1 from rat anterior pituitary tissues perifused in vitro. These findings suggest that ECT suppresses GH secretion in the rat, at least in part, through the central nervous system.