Niebler M, Trendelenburg U
Institut für Pharmakologie und Toxikologie, Universität Würzburg, Federal Republic of Germany.
Naunyn Schmiedebergs Arch Pharmacol. 1990 Jan-Feb;341(1-2):43-9. doi: 10.1007/BF00195056.
In the rat vas deferens, DMPP is a substrate of uptake1 (Km = 11.5 mumol/l). After block of vesicular uptake, monoamine oxidase and catechol-O-methyl transferase, after loading of the tissue with 3H-noradrenaline, and in calcium-free solution (i.e., when axoplasmic 3H-noradrenaline levels were high and when depolarization-induced exocytotic release was impossible), DMPP induced a pronounced outward transport of 3H-noradrenaline. On the other hand, when, in similar experiments, vesicular uptake and monoamine oxidase were intact (i.e., when axoplasmic 3H-noradrenaline levels were low), DMPP induced very little outward transport of 3H-noradrenaline. This discrepancy indicates that DMPP has little ability to mobilize vesicularly stored 3H-amine. When the medium contained calcium (catechol-O-methyl transferase inhibited, all other mechanisms intact), 100 (but not 10) mumol/l DMPP induced a hexamethonium-sensitive release of 3H-noradrenaline of short duration. Hence, in the presence of extracellular calcium, 100 mumol/l DMPP elicits exocytotic release via activation of hexamethonium-sensitive nicotinic acetylcholine receptors. DMPP inhibits the monoamine oxidase of rat heart homogenate with an IC50 of about 100 mumol/l.
在大鼠输精管中，二甲基苯基哌嗪（DMPP）是摄取1的底物（米氏常数Km = 11.5 μmol/L）。在用3H-去甲肾上腺素使组织负载后，在无钙溶液中（即当轴浆中3H-去甲肾上腺素水平较高且去极化诱导的胞吐释放不可能发生时），阻断囊泡摄取、单胺氧化酶和儿茶酚-O-甲基转移酶后，DMPP诱导了显著的3H-去甲肾上腺素外向转运。另一方面，在类似实验中，当囊泡摄取和单胺氧化酶完整时（即当轴浆中3H-去甲肾上腺素水平较低时），DMPP诱导的3H-去甲肾上腺素外向转运非常少。这种差异表明DMPP动员囊泡储存的3H-胺的能力很小。当培养基中含有钙时（儿茶酚-O-甲基转移酶被抑制，所有其他机制完整），100（而非10）μmol/L的DMPP诱导了持续时间较短的对六甲铵敏感的3H-去甲肾上腺素释放。因此，在细胞外钙存在的情况下，100 μmol/L的DMPP通过激活对六甲铵敏感的烟碱型乙酰胆碱受体引发胞吐释放。DMPP抑制大鼠心脏匀浆的单胺氧化酶，半数抑制浓度（IC50）约为100 μmol/L。
