Role of brain adrenoceptors in the corticortopin-releasing factor-induced central activation of sympatho-adrenomedullary outflow in rats

We investigated the role played by catecholamine-dependent pathways in modulating the ability of centrally administered corticotropin releasing factor (CRF) to activate sympatho-adrenomedullay outflow, using urethane-anesthetized rats. The CRF (1.5 nmol/animal, i.c.v.)-induced elevations of both plasma noradrenaline and adrenaline were attenuated by phentolamine (a non-selective α adrenoceptor antagonist) [125 and 250 µg (0.33 and 0.66 µmol)/animal], Heat (a selective α1 adrenoceptor antagonist) [10 and 30 µg (30 and 90 nmol)/animal, i.c.v.] and clonidine (a selective α2 adrenoceptor agonist) [100 µg (0.375 µmol)/animal, i.c.v.]. On the other hand, the CRF (1.5 nmol/animal, i.c.v.)-induced elevation of both catecholamines was not influenced by RS 79948 (a selective α2 adrenoceptor antagonist) [10 and 30 µg (7.2 and 72 nmol)/animal, i.c.v.]. Furthermore, the CRF (1.5 nmol/animal, i.c.v.)-induced elevation of noradrenaline was attenuated by sotalol (a non-selective β adrenoceptor antagonist) [125 and 250 µg (0.4 and 0.8 µmol)/animal, i.c.v.], while that of adrenaline was not influenced by sotalol. These results suggest that centrally administered CRF-induced elevation of plasma noradrenaline is mediated by an activation of α1 and β adrenoceptors in the brain, and that of plasma adrenaline is mediated by an activation of α1 adrenoceptors in the brain. Furthermore, central α2 adrenoceptors are involved in modulating the CRF-induced elevation of both plasma catecholamines.