Zebrowska-Lupina I, Szurska G
Pol J Pharmacol Pharm. 1986 May-Jun;38(3):243-9.
The influence of phenylephrine (PHE), methoxamine (MET) and ephedrine (EPH) on kininogen and prekallikrein level in plasma was investigated in male Wistar rats. Simultaneously the effect of these drugs on blood pressure was monitored. No changes in kininogenesis were observed during the hypertension period (2 h after ip injection). The significant decrease in kininogen level (by 20-30%) was found 4 h after PHE (5 mg/kg) or EPH (40 mg/kg) and 4-12 h after MET (40 mg/kg) injection. The reduction of kallikrein utilization, indicating an increase in prekallikrein level in plasma, was noted only after PHE (by 34%) or MET (by 44%) administration. Phentolamine (REG) in a dose of 20 mg/kg, which counteracted the hypertensive effect of investigated drugs, abolished the influence of these drugs on kininogen level. The results indicate that the hypertension induced by alpha-adrenoceptor agonists evokes the delayed activation of kininogenesis parallel to the secondary decrease in blood pressure. Such a reaction of kinin system seems to be related to primary alpha-adrenoceptor stimulation, not to the direct influence of hypertensive drugs on kinin system in rat plasma.
在雄性Wistar大鼠中研究了去氧肾上腺素（PHE）、甲氧明（MET）和麻黄碱（EPH）对血浆中激肽原和前激肽释放酶水平的影响。同时监测了这些药物对血压的影响。在高血压期（腹腔注射后2小时）未观察到激肽生成的变化。在注射PHE（5毫克/千克）或EPH（40毫克/千克）后4小时以及注射MET（40毫克/千克）后4至12小时，发现激肽原水平显著降低（降低20%至30%）。仅在给予PHE（降低34%）或MET（降低44%）后，才注意到激肽释放酶利用率降低，这表明血浆中前激肽释放酶水平升高。剂量为20毫克/千克的酚妥拉明（REG）可抵消所研究药物的高血压作用，消除这些药物对激肽原水平的影响。结果表明，α-肾上腺素能受体激动剂诱导的高血压会引发激肽生成的延迟激活，同时血压继发性降低。激肽系统的这种反应似乎与原发性α-肾上腺素能受体刺激有关，而不是与高血压药物对大鼠血浆中激肽系统的直接影响有关。
