Propofol differentially attenuates the responses to exogenous and endogenous norepinephrine in the isolated rat femoral artery in vitro.

Propofol causes a decrease in vascular resistance mediated in part by a decrease in sympathetic output. To determine whether attenuation of norepinephrine release from sympathetic perivascular nerve terminals could contribute to decreased vascular resistance, we examined the effects of propofol on the contractile responses to exogenous and endogenous norepinephrine in the rat femoral artery. Endogenous norepinephrine was released from sympathetic nerve terminals using electrical field stimulation. The responses to both exogenous norepinephrine and neurally released norepinephrine were attenuated by propofol in concentrations from 1.0 to 10.0 micrograms/mL. At 50% of maximal and at maximal contractile responses to norepinephrine and electrical field stimulation, the response to electrical field stimulation was inhibited to a greater extent than the response to exogenous norepinephrine. This suggests that, in addition to direct postsynaptic vasodilation, propofol has the presynaptic effect of inhibiting norepinephrine release from perivascular nerves.