Role of brain histamine on corticosteroid release

Abstract

There is a considerable amount of literature that described how parenteral injection of histamine stimulates adrenocortical secretion in dogs and rats (Katsuki et al., 1967; Hirose et al., 1976; Cowan, 1975; Reilly, 1984), but few experiments have been done to clarify the role of brain histamine in releasing corticosteroids. Parenteral administration of histamine induces some side effects such as hypotensive effect and algesia, and these responses undoubtedly exert some influence on the pituitary-adrenocortical axis and adrenal steroid release. Since histamine does not enter into the brain through the blood-brain barrier, intracerebroventricular (i.c.v.) injection has been commonly employed to study the histamine effect on the central nervous system (CNS) (Feldberg and Sherwood, 1954; Tasaka et al., 1989). Rudolph et al. (1979) reported that activation of central H₁ receptors increases ACTH secretion in dogs, and that activation of central H₂ receptors decreases ACTH secretion. On the contrary, in rats, Bugajski and Gadek (1983) reported that i.c.v. injection of histamine increased plasma.corticosterone concentrations and this effect was mediated by both H₁ and H₂ receptors. From these findings, it seems likely that species difference exists between dogs and rats in histamine-induced corticosteroid release especially in the participation of H₂ receptors. Recently, the presence of the H₃ receptors, which is responsible for the feedback control of histamine synthesis and release, has also been demonstrated (Arrang et al., 1987). However, it is not known whether or not the H₃ receptor is involved in histamine-induced steroidogenesis.