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Prince Henry’s Institute of Medical Research, Clayton, Australia

(Requests for offprints should be addressed to C Chen, Prince Henry’s Institute of Medical Research, P O Box 5152, Clayton, Victoria 3168, Australia; Email: chen.chen{at}phimr.monash.edu.au)

Activin A is a member of the transforming growth factor-ß family and has known roles in the adrenal cortex, from which activin A is secreted. We aimed to find whether activin A induces secretion of catecholamines from chromaffin cells of the adrenal medulla, which neighbours the adrenal cortex in vivo. Using carbon fibre amperometry, we were able to measure catecholamine secretion in real-time from single chromaffin cells dissociated from the rat adrenal medulla. Activin A stimulated catecholamine secretion in a rapid and dose-dependent manner from chromaffin cells. This effect was fully reversible upon washout of activin A. The minimum dose at which activin A had a maximal effect was 2 nM, with an EC₅₀ of 1.1 nM. The degree of secretion induced by activin A (2 nM) was smaller than that due to membrane depolarization caused by an increase in the external K⁺ concentration from 5 to 70 mM. No response to activin A was seen when Ca²⁺ channels were blocked by Cd²⁺ (200 µM). We conclude from these findings that activin A is capable of stimulating a robust level of catecholamine secretion from adrenal chromaffin cells in a concentration-dependent manner. This occurs via the opening of voltage-gated Ca²⁺ channels, causing Ca²⁺ entry, thereby triggering exocytosis. These findings illustrate a new physiological role of activin A and a new mechanism in the control of catecholamine secretion from the adrenal medulla.