Upregulation of adrenocorticotrophic hormone in the corticotrophs and downregulation of surface receptors and antigens on the macrophages in the adenohypophysis following an exposure to high altitude.

Abstract Altitude exposures lead to the development of hypobaric hypoxia because of low oxygen tension in the ambient air. This study has shown the vigorous upregulation of adrenocorticotrophic hormone (ACTH) expression in corticotrophs of the pars distalis (adenohypophysis) of rats 1–7 days after an altitude exposure. Concomitant to this was the increase in number and hypertrophy of the immunoreactive corticotrophs. It was suggested that this had resulted in an upsurge of ACTH production which may have suppressed the immuno-expression of complement type 3 receptors and major histocompatibility complex class II antigens constitutively expressed by the parenchymal macrophages through paracrine action. Along with ACTH, altered levels of other hormones following such exposures may also contribute to suppression of antigen presenting function and phagocytic activity of macrophages. The effects of altitude (hypobaric hypoxia) exposure, however, were reversible as the above immunohistochemical changes returned to normal 21–28 days after the hypobaric hypoxic insult.