Morelowska D, Chabielska E, Pawlak D, Azzadin A, Białkowska A, Krygicz D, Buczko W
Department of Pharmacodynamics, Medical Academy, Białystok, Poland.
Pol J Pharmacol Pharm. 1992 Jul-Aug;44(4):365-72.
In 2K,1C-RHR (two-kidney, one-clip hypertensive rats) serotonergic mechanisms in blood platelets were studied. The endogenous serotonin (5-HT) concentration in whole blood and in platelets remained unchanged in relation to the sham operated rats. Also the uptake of labelled 5-HT in rats with renal hypertension was not altered. However platelets aggregability was increased in 2K,1C-RHR. Acute administration of captopril (10 mg/kg and 100 mg/kg po) diminished blood pressure but did not change either the concentration of 5-HT in whole blood and in platelets of hypertensive rats or the uptake of this amine. Platelets aggregation and the amplifying effect of 5-HT in hypertensive rats were also unchanged after acute captopril administration. Similar results were observed after its administration in a dose of 30 mg/kg for one week. Our results indicate that captopril did not affect the platelets serotonergic mechanisms in 2K,1C-RHR.
对两肾一夹高血压大鼠(2K,1C-RHR)血小板中的5-羟色胺能机制进行了研究。与假手术大鼠相比,全血和血小板中内源性5-羟色胺(5-HT)浓度保持不变。此外,肾性高血压大鼠对标记5-HT的摄取也未改变。然而,2K,1C-RHR大鼠的血小板聚集性增加。急性给予卡托普利(10毫克/千克和100毫克/千克,口服)可降低血压,但对高血压大鼠全血和血小板中5-HT的浓度或该胺的摄取均无影响。急性给予卡托普利后,高血压大鼠的血小板聚集以及5-HT的放大作用也未改变。以30毫克/千克的剂量给药一周后观察到类似结果。我们的结果表明,卡托普利不影响2K,1C-RHR大鼠血小板中的5-羟色胺能机制。