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 alpha adrenoceptor antagonist) [125 and 250 mu g (0.33 and 0.66 mu mol)/animal], Heat (a selective alpha(1) adrenoceptor antagonist) [10 and 30 mu g (30 and 90 nmol)/animal, i.c.v.] and clonidine (a selective alpha(2) adrenoceptor agonist) [100 mu g (0.375 mu mol)/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 alpha(2) adrenoceptor antagonist) [10 and 30 mu g (7.2 and 72 nmol)/animal, i.c.v.]. Furthermore, the CRF (1.5 nmol/animal, i.e.v.)-induced elevation of noradrenaline was attenuated by sotalol (a non-selective adrenoceptor antagonist) [125 and 250 mu g (0.4 and 0.8 mu mol)/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 a, and beta adrenoceptors in the brain, and that of plasma adrenaline is mediated by an activation of alpha(1) adrenoceptors in the brain. Furthermore, central alpha(2) adrenoceptors are involved in modulating the CRF-induced elevation of both plasma catecholamines. (c) 2007 Elsevier Inc. All rights reserved.