Pharmacological differences between neurogenic sympathetic responses in rat and pig isolated pulmonary arteries were examined in strip preparations. Electrical field stimulation in the range of 0.6 to 40 Hz resulted in frequency-dependent contractions in terms of amplitude and rate of rise. Responses in the rat declined sharply from pulmonary trunk to main artery; in contrast, in the pig they continued into the third-order vessels. Contractions were inhibited in the presence of tetrodotoxin, prazosin or WB-4101 and hence neurogenic in origin. Cocaine enhanced field stimulated contractions in both rat and porcine tissues; however, the effect in the former was of significantly greater magnitude in terms of either area under the mechanogram or height of contraction. In addition, the rate of rise, time to peak and duration of peak were all increased in the rat but less so or not in the pig. Field stimulated contractions were virtually abolished by guanethidine (1×10−6 M) in rat but not in porcine pulmonary arteries in which a ten-fold higher concentration significantly reduced neurogenic contractions and abolished them in 2 out of 4 tissues tested. The effect of guanethidine (1×10−6 M) observed in blood vessels of rat exceeded about five-fold that observed in porcine tissues. Thus, neurogenic responses appear to be entirely mediated by extra-junctional α1-adrenoceptors in both species, and in contrast to the rat, pig tissues seem to have a noradrenaline re-uptake that is either less efficient or operating near saturation.