The hypotensive effect of DC-015, a newly synthesized quinazoline derivative, was investigated and compared with prazosin in spontaneously hypertensive rats (SHR). Intravenous administration of DC-015 and prazosin (both at 0.01, 0.05 and 0.1 mg/kg) induced a dose-dependent reduction of mean arterial pressure (MAP) which reached a maximal effect at 5 min after injection and persisted over 2 h in SHR. Furthermore, at higher doses DC-015 (0.1 mg/kg i.v. and 2.0 mg/kg orally, respectively) did not cause any significant changes in heart rate (HR); whereas the same doses of prazosin (0.1 mg/kg i.v. and 2.0 mg/kg orally, respectively) produced a decrease in HR which seems to parallel the time course of the hypotensive response in SHR. DC-015 and prazosin attenuated pressor responses to phenylephrine (10 &mgr;g/kg) but failed to inhibit the pressor effects of angiotensin II (0.5 &mgr;g/kg) even at the maximal hypotensive dose (0.1 mg/kg). This observation indicates that DC-015 appears to exert its hypotensive effect through alpha(1)-adrenoceptor blockade. On the other hand, in SHR fed a high-fat-high-cholesterol (HF-HC) diet, oral administration of DC-015 and prazosin (both at 1.0 mg/kg, twice a day) for 4 weeks caused significant reductions in total plasma cholesterol (CE), low-density lipoprotein (LDL)-cholesterol and total plasma triglyceride (TG). DC-015 therapy also increased high-density lipoprotein (HLD)-cholesterol levels, thus the ratio of total plasma cholesterol to HDL-CE was improved. In contrast, prazosin did not significantly increase the HDL-CE level in this study. It is concluded that DC-015 decreased MAP, plasma CE, LDL-CE, plasma TG and increased HDL-CE levels. DC-015 may have therapeutic potential as a potent antihypertensive drug via the alpha(1)-adrenoceptor antagonist. Concurrently, DC-015 may thus hold some advantage for the reduction of two of the major risk factors, hypertension and hyperlipidemia, for cardiovascular diseases. Copyright 1996 S. Karger AG, Basel

译文

:对新合成的喹唑啉衍生物DC-015的降压作用进行了研究,并与哌唑嗪在自发性高血压大鼠(SHR)中进行了比较。静脉内施用DC-015和哌唑嗪(分别为0.01、0.05和0.1 mg / kg)导致剂量依赖性平均动脉压(MAP)降低,在注射后5分钟达到最大作用,并在SHR中持续2小时以上。此外,在较高剂量下,DC-015(静脉内分别为0.1 mg / kg和2.0 mg / kg口服)不会引起心率(HR)的任何显着变化;而相同剂量的哌唑嗪(分别为0.1 mg / kg静脉内和2.0 mg / kg口服)可导致HR降低,这似乎与SHR中降压反应的时间过程一致。 DC-015和哌唑嗪减弱了对去氧肾上腺素(10μg/ kg)的升压反应,但即使在最大降压剂量(0.1 mg / kg)下也未能抑制血管紧张素II(0.5μg/ kg)的升压作用。该观察结果表明DC-015似乎通过α(1)-肾上腺素受体阻滞发挥其降压作用。另一方面,在以高脂高胆固醇(HF-HC)饮食喂养的SHR中,口服DC-015和哌唑嗪(1.0 mg / kg,每天两次),持续4周,可导致SHR的显着降低。总血浆胆固醇(CE),低密度脂蛋白(LDL)-胆固醇和总血浆甘油三酸酯(TG)。 DC-015治疗还增加了高密度脂蛋白(HLD)-胆固醇的水平,因此总血浆胆固醇与HDL-CE的比率得到了改善。相反,在本研究中,哌唑嗪并未显着增加HDL-CE水平。结论是DC-015降低MAP,血浆CE,LDL-CE,血浆TG和增加HDL-CE水平。 DC-015通过α(1)-肾上腺素受体拮抗剂可能作为强效降压药具有治疗潜力。同时,DC-015因此对于减少心血管疾病的两个主要危险因素高血压和高脂血症可能具有一定的优势。版权所有1996 S. Karger AG,巴塞尔

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