Abstract

The constrictor response to extraluminal norepinephrine (NE) was altered in two ways by nialamide treatment: 1) the primary steady state was followed by a slowly developing secondary increase in the magnitude of the response and 2) recovery after washout of the NE was delayed. Arteries which were chronically denervated or which were exposed to cocaine and NE simultaneously did not display the secondary response or delayed recovery. Although the effects of the latter treatments on the secondary response may have been related to the concentration of NE, this possibility was excluded in the case of delayed recovery by the use of equal concentrations of NE (0.5 µg/ml). These results suggest that delay in recovery is associated with inhibition of intraneuronal rather than extraneuronal monoamine oxidase. In contrast to its effects of extraluminal NE, nialamide treatment did not affect the time course of the response to intraluminal NE or recovery from this response. The difference is attributed to a relative failure on the part of intraluminal NE to penetrate to the sympathetic nerve terminals. Nialamide treatment had little effect on the magnitudes of time primary steady-state responses to intraluminal and to extraluminal NE in both innervated and chronically denervated arteries. The failure of nialamide to modify either the magnitude of the response to intraluminal NE or recovery from this response is a further indication that inactivation of NE by extraneuronal monoamine oxidase is of little functional importance in this artery.