Hypothalamic adrenoceptors mediate sympathoadrenal activity in exercising rats

The role of hypothalamic adrenoceptors in the exercise-induced alterations of plasma norepinephrine (NE), epinephrine (E), and corticosterone concentrations was investigated in rats. Exercise consisted of strenuous swimming against a countercurrent for 15 min. Before, during, and after swimming, blood samples were withdrawn through a permanent heart catheter for determination of E, NE, and corticosterone. In control rats E, NE, and corticosterone levels were all increased during exercise. Infusion of the ar-adrenoceptor antagonist phentolamine through permanent bilateral cannulas into the ventromedial hypothalamus (VMH) immediately before exercise reduced the exercise-induced increase in plasma E without affecting NE. Infusion of the β-adrenoceptor antagonist timolol into the VMH enhanced plasma E and attenuated plasma NE increases. Infusion of phentolamine into the lateral hypothalamic area (LHA) led to enhanced NE and unchanged E concentrations, whereas infusion of timolol into the LHA caused a potentiation of the increase in plasma E without an effect on NE. Plasma corticosterone concentrations were not affected. The results suggest that 1) α- and β-adrenoceptors in the hypothalamus influence peripheral catecholamine release, and 2) E and NE responses to exercise can be dissociated by interference of the central nervous system.