Inhibition by (−)‐Deprenyl of Agonist‐Evoked Contractions in Rabbit Aorta

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Abstract
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 × 10−4M) antagonized the contractions evoked by noradrenaline (10−8−3 × 10−4M); pA2: 5.10. The antagonism was reversible. It was attenuated by cocaine (3x M); pA2: 4.38, unchanged by corticosterone (4 × 10−5M); pA24.79 and enhanced by cocaine (3 × 10−5M) plus corticosterone (4 × 10−5M); pA2: 5.48. (+)‐Deprenyl (10−6−10−4M) did not alter the contractions evoked by noradrenaline (3 × 10−9−10−4M). Clorgyline (10−5and 10−4M) antagonized the noradrenaline‐evoked contractions. Pargyline (10−4and 3 × 10−4M) had no effect. (−)‐Deprenyl (10−5−3 × 10−4M) antagonized the contractions evoked by phenylephrine (10−8−10−4M); pA2: 5.10. Removal of the endothelium did not alter the antagonism; pA2: 5.35. (−)‐Deprenyl (10−5−3 × 10−4M) antagonized the contractions evoked by either 5‐hydroxytryptamine (3 × 10−8−3 × 10−4M); pA2: 4.61 or by histamine (10−6−3 × 10−2M); pA2: 4.84. (−)‐Deprenyl (3 × 10−4M) caused a non‐competitive antagonism of the contractions evoked by potassium (1.5‐5.5 × 10−2M). It is concluded that (−)‐deprenyl is a weak inhibitor of postjunctional α‐adrenoceptors, 5‐hydroxytryptamine (5‐HT2) receptors, and histamine (H1) receptors.