Abstract

Sympathetic reflexes in an in vitro frog spinal cord appeared to be qualitatively similar to those observed in cats in vivo. The present study ws conducted to determine whether or not this similarity extended to catecholamine effects on spinal sympathetic reflexes and to examine the adrenoceptor mechanisms responsible for these effects. Norepinephrine inhibited spinal sympathetic reflexes elicited by supramaximal electrical stimulation of the second spinal nerve in a concentration-dependent manner. This inhibition could be mimicked by other alpha adrenoceptor agonists and was antagonized by phentolamine. No effect of norepinephrine was observed when submaximal stimuli were employed. Epinephrine facilitated reflex activity elicited by both submaximal and supramaximal stimulation; however, in the presence of propranolol, an inhibitory effect of epinephrine was observed. At high concentrations, dopamine inhibited spinal sympathetic reflex activity and this inhibition was antagonized by phentolamine. l-Dopa produced a slow-onset, long-lasting inhibition which could be blocked by pretreatment with a decarboxylase inhibitor. It is concluded that alpha adrenoceptor agonists acting on alpha receptors can inhibit spinal sympathetic reflex activity and that the inhibition is dependent on the intensity of stimulation. Activation of beta adrenoceptors facilitates, whereas activation of dopamine receptors has no effect on, spinal sympathetic reflexes. These alpha and beta adrenoceptor mechanisms may function in the modulation of sympathetic preganglionic activity in the intact animal.