Inhibition by (-)-deprenyl of agonist-evoked contractions in rabbit aorta

The effect of (-)-deprenyl, a relatively selective MAO-B inhibitor, was examined for its ability to inhibit the contractions of rabbit isolated aorta evoked by various agonists and potassium. (-)-Deprenyl (10(-5)-3 x 10(-4) M) antagonized the contractions evoked by noradrenaline (10(-8)-3 x 10(-4) M); pA2: 5.10. The antagonism was reversible. It was attenuated by cocaine (3 x 10(-5) M); pA2: 4.38, unchanged by corticosterone (4 x 10(-5) M); pA2 4.79 and enhanced by cocaine (3 x 10(-5) M) plus corticosterone (4 x 10(-5) M); pA2: 5.48. (+)-Deprenyl (10(-6)-10(-4) M) did not alter the contractions evoked by noradrenaline (3 x 10(-9)-10(-4) M). Clorgyline (10(-5) and 10(-4) M) antagonized the noradrenaline-evoked contractions. Pargyline (10(-4) and 3 x 10(-4) M) had no effect. (-)-Deprenyl (10(-5)-3 x 10(-4) M) antagonized the contractions evoked by phenylephrine (10(-8)-10(-4) M); pA2: 5.10. Removal of the endothelium did not alter the antagonism; pA2: 5.35. (-)-Deprenyl (10(-5)-3 x 10(-4) M) antagonized the contractions evoked by either 5-hydroxytryptamine (3 x 10(-8)-3 x 10(-4) M); pA2: 4.61 or by histamine (10(-6)-3 x 10(-2) M); pA2: 4.84. (-)-Deprenyl (3 x 10(-4) M) caused a noncompetitive antagonism of the contractions evoked by potassium (1.5-5.5 x 10(-2) M). It is concluded that (-)-deprenyl is a weak inhibitor of postjunctional alpha 1-adrenoceptors, 5-hydroxytryptamine (5-HT2) receptors, and histamine (H1) receptors.