The stress hormone adrenocorticotropin enhances sympathetic outflow to the muscle vascular bed in humans.

OBJECTIVE

To examine the role of adrenocorticotropin in the regulation of the sympathetic outflow to the muscle vascular bed in healthy female humans.

DESIGN

Eight healthy, nonsmoking female subjects (aged 18-33 years) were examined before and after injection of 0.25 mg adrenocorticotropin 1-24 or placebo according to a balanced, double-blind cross-over protocol.

METHODS

Muscle sympathetic nerve activity, arterial pressure, and heart rate were continuously recorded both under basal conditions and during a 50 min period after injection of each substance. Furthermore, sympathoexcitatory capacities of inspiratory apneas and cold pressure tests performed before and after injection of adrenocorticotropin were determined.

RESULTS

The injection of adrenocorticotropin rapidly increased burst frequency of muscle sympathetic nerve activity (P < 0.01). The maximal effect of adrenocorticotropin, with an increase in burst frequency of 63%, occurred during the third minute after injection and waned subsequently, but muscle sympathetic nerve activity remained significantly increased during the first 10 min after injection. The stimulatory effect of adrenocorticotropin had disappeared 40 min after injection. The sympathoexcitatory capacity of a maximal inspiratory apnea and a cold pressure test, respectively, remained unchanged 10 and 45 min after the administration of adrenocorticotropin compared with control. Neither blood pressure nor heart rate was significantly affected by administration of the peptide.

CONCLUSIONS

The data establish that the stress hormone adrenocorticotropin acutely increases sympathetic outflow to the muscle vascular bed in female humans. This effect is most likely mediated via central nervous system autonomic centers. The influence of adrenocorticotropin on the sympathetic nervous system might contribute to the alteration of response to stress in the course of the development of hypertension and could also add to the hypertensiogenic effects of corticosteroids and mineralocorticoids in states with excess adrenocorticotropin.