Cervoni P, Herzlinger H E, Lai F M, Tanikella T K
Br J Pharmacol. 1983 Jul;79(3):667-71. doi: 10.1111/j.1476-5381.1983.tb10003.x.
The effects of (+/-)-1-O-octadecyl-2-acetyl-glyceryl-3-phosphorylcholine (octadecyl-AGPC) were studied in three types of aortic vascular smooth muscle preparations, namely, strips, rubbed and unrubbed rings, and an atrial preparation in normotensive rats. In the resting tension state, octadecyl-AGPC did not elicit significant contractions in either rubbed or unrubbed ring preparations at concentrations lower than 1 X 10(-4) M. However, at a concentration of 3 X 10(-4) M, octadecyl-AGPC markedly contracted both types of ring preparations. This contractile response was partially antagonized by pretreatment with reserpine and completely blocked by phentolamine (1 X 10(-6) M). In preparations contracted with noradrenaline (NA), octadecyl-AGPC elicited biphasic responses in intact ring preparations; an initial relaxation followed by contraction. Octadecyl-AGPC induced only a slight contraction in strips and a slight relaxation in the rubbed ring preparation. Octadecyl-AGPC did not elicit any significant effect on chronotropy or inotropy at concentrations up to 3 X 10(-5) M. When the concentration was 1 X 10(-4) M, octadecyl-AGPC produced significant positive chronotropic and inotropic effects on spontaneously beating right and electrically driven left atrial preparations, respectively. Both effects were blocked by propranolol (5 X 10(-8) M); reserpine pretreatment antagonized only the chronotropic response. In [3H]-dihydroalprenolol [( 3H]-DHA) binding studies, octadecyl-AGPC had a Kd of 427.85 microM and thus was much less potent than isoprenaline (Kd = 465.10 nM) or propranolol (Kd = 4.4 nM) in displacing [3H]-DHA in rat cardiac membrane preparations. 6 In conclusion, relaxation and contraction induced by octadecyl-AGPC in aortic preparations is an indirect rather than a direct effect. An unknown factor released from endothelial cells is responsible for aortic smooth muscle relaxation by octadecyl-AGPC while released NA appears to be responsible for aortic vascular contraction and for the positive chronotropic and inotropic effects in the atrial preparations.
研究了（±）-1-O-十八烷基-2-乙酰基甘油-3-磷酸胆碱（十八烷基-AGPC）对正常血压大鼠的三种主动脉血管平滑肌制剂的作用，即条带、摩擦和未摩擦的环以及心房制剂。在静息张力状态下，当浓度低于1×10⁻⁴M时，十八烷基-AGPC在摩擦或未摩擦的环制剂中均未引起明显收缩。然而，在浓度为3×10⁻⁴M时，十八烷基-AGPC使两种类型的环制剂均明显收缩。这种收缩反应部分被利血平预处理拮抗，而被酚妥拉明（1×10⁻⁶M）完全阻断。在与去甲肾上腺素（NA）收缩的制剂中，十八烷基-AGPC在完整的环制剂中引起双相反应；先是舒张，随后是收缩。十八烷基-AGPC在条带中仅引起轻微收缩，在摩擦的环制剂中引起轻微舒张。在浓度高达3×10⁻⁵M时，十八烷基-AGPC对变时性或变力性均未引起任何明显影响。当浓度为1×10⁻⁴M时，十八烷基-AGPC分别对自发搏动的右心房制剂和电驱动的左心房制剂产生明显的正性变时性和变力性作用。两种作用均被普萘洛尔（5×10⁻⁸M）阻断；利血平预处理仅拮抗变时性反应。在[³H]-二氢阿普洛尔（[³H]-DHA）结合研究中，十八烷基-AGPC的解离常数（Kd）为427.85μM，因此在大鼠心脏膜制剂中取代[³H]-DHA的效力远低于异丙肾上腺素（Kd = 465.10 nM）或普萘洛尔（Kd = 4.4 nM）。总之，十八烷基-AGPC在主动脉制剂中引起的舒张和收缩是间接而非直接作用。内皮细胞释放的未知因子负责十八烷基-AGPC引起的主动脉平滑肌舒张，而释放的NA似乎负责主动脉血管收缩以及心房制剂中的正性变时性和变力性作用。
