Differential effect of propofol on sympathetic neurotransmission in isolated human omental arteries and veins

1 The present study was undertaken to elucidate the effect of propofol on sympathetic neurotransmission in isolated human omental vessels. 2 Segments of both arteries and veins were exposed to 0, 10 −7 , 10 −6 , 10 −5 or 10 −4   M propofol, and studied in vitro to determine effects on: (i) isometric tension after electrical field stimulation (EFS) or after exogenous administration of noradrenaline (NA); (ii) EFS‐stimulated release of [ 3 H]‐NA from vessel segments preincubated with [ 3 H]‐NA; (iii) uptake of [ 3 H]‐NA. 3 Propofol at 10 −6   M enhanced EFS‐induced contraction in artery segments, 10 −7 and 10 −5   M had no effect, and 10 −4   M propofol depressed EFS‐induced contraction in both artery and vein segments. 4 Propofol did not affect the response to exogenous NA in artery and vein segments. 5 EFS‐stimulated release of [ 3 H]‐NA was depressed by 10 −5 and 10 −4   M propofol in artery segments, and by 10 −4   M in vein segments. 6 Uptake of [ 3 H]‐NA was depressed by 10 −6 –10 −4   M propofol in artery but not in vein segments. 7 The results suggest that sympathetic neurotransmission is enhanced at clinical concentrations (10 −6   M ) of propofol in human omental arteries, but not veins. This may be due to an increased availability of NA in the neuromuscular junction resulting from a reduced presynaptic reuptake. Propofol at probably supraclinical concentrations (10 −5 –10 −4   M ) impairs the sympathetic neurotransmission in both human omental arteries and veins, probably due to an inhibitory effect on the NA release from the sympathetic nerves.British Journal of Pharmacology (1998) 125 , 120–126; doi: 10.1038/sj.bjp.0702021