Prolonged kallikrein inhibition does not affect the basal growth end secretory capacity of rat adrenal cortex, but enhances mineralo- and glucocorticoid response to ACTH and handling stress

The effects on the pituitary-adrenocortical functions of the prolonged (7-d ay) blockade of endogenous bradykinin (BK) synthesis, obtained by the admin istration of the kallikrein inhibitor (K-I) cyclohexylacetyl-Phe-Arg-Ser-Va l-Gln amide, were investigated in the rat. K-I treatment did not cause sign ificant changes in the (i) body and adrenal weights; (ii) basal plasma leve ls of ACTH, aldosterone and corticosterone; and (iii) average volume of adr enocortical cells and their basal secretory capacity. Conversely, K-I admin istration induced a significant magnification of the in vivo mineralo- and glucocorticoid responses to the intraperitoneal (i.p.) bolus injection of A CTH. Moreover, K-I-treated rats, but not control ones, displayed a moderate and short-term adrenal secretory response to the mild stress evoked by the placebo i.p. injection. Collectively, these findings rule out the possibil ity that endogenous BK plays a relevant role in the control of adrenocortic al function under basal conditions. However, they suggest that endogenous B K may be involved in quenching exceedingly high adrenocortical responses to ACTH and stresses.