Nedergaard O A, Møller J
Department of Pharmacology, School of Medicine, Odense University, Denmark.
Pharmacol Toxicol. 1994 Dec;75(6):377-83. doi: 10.1111/j.1600-0773.1994.tb00378.x.
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.
研究了相对选择性的单胺氧化酶-B（MAO-B）抑制剂（-）-司来吉兰抑制多种激动剂和钾离子诱发的兔离体主动脉收缩的能力。（-）-司来吉兰（10^-5 - 3×10^-4 M）拮抗去甲肾上腺素（10^-8 - 3×10^-4 M）诱发的收缩；pA2为5.10。这种拮抗作用是可逆的。可卡因（3×10^-5 M）可减弱该拮抗作用；pA2为4.38，皮质酮（4×10^-5 M）对其无影响；pA2为4.79，而可卡因（3×10^-5 M）加皮质酮（4×10^-5 M）可增强该拮抗作用；pA2为5.48。（+）-司来吉兰（10^-6 - 10^-4 M）不改变去甲肾上腺素（3×10^-9 - 10^-4 M）诱发的收缩。氯吉兰（10^-5和10^-4 M）拮抗去甲肾上腺素诱发的收缩。帕吉林（10^-4和3×10^-4 M）无作用。（-）-司来吉兰（10^-5 - 3×10^-4 M）拮抗苯肾上腺素（10^-8 - 10^-4 M）诱发的收缩；pA2为5.10。去除内皮不改变该拮抗作用；pA2为5.35。（-）-司来吉兰（10^-5 - 3×10^-4 M）拮抗5-羟色胺（3×10^-8 - 3×10^-4 M）或组胺（10^-6 - 3×10^-2 M）诱发的收缩；pA2分别为4.61和4.84。（-）-司来吉兰（3×10^-4 M）对钾离子（1.5 - 5.5×10^-2 M）诱发的收缩产生非竞争性拮抗作用。结论是（-）-司来吉兰是一种弱的节后α1-肾上腺素能受体、5-羟色胺（5-HT2）受体和组胺（H1）受体抑制剂。
