Costa M A, Balaszczuk A M, Domínguez A, Catanzaro O, Arranz C
Departamento de Ciencias Biológicas, Facultad de Farmacia y Bioquimíca, Universidad de Buenos Aires, Capital Federal, Argentina.
Acta Physiol Pharmacol Ther Latinoam. 1998;48(2):59-63.
The present study was designed to examine blood pressure response to nitric oxide synthase-pathway inhibition and stimulation in normotensive and hypertensive diabetic rats. Rats treated with streptozotocin (60 mg/Kg i.p.) developed high blood glucose, polyuria and slow weight gain compared with control. One group of diabetic rats developed hypertension, consequently we studied three experimental groups: control rats (C), normotensive diabetic rats (ND) and hypertensive diabetic rats (HD). Mean arterial pressure (MAP), systolic blood pressure, diastolic blood pressure and heart rate were recorded: baseline time, 30 after L-nitro arginine methyl ester (L-NAME: 1 mg/Kg i.v.) and post L-arginine (L-arg: 250 mg/Kg i.v.) injection. L-NAME induced a significantly increase in MAP in all groups. This enhancement was smaller in diabetic than in control rats. The increase in MAP in HD was significantly lower than that in ND L-arg induced a significantly decrease in MAP in all groups. This decrease was significantly attenuated in diabetic compared with control rats. The degree of hypotension in response to L-arg in diabetic groups was lower in hypertensive than that in normotensive diabetic rats. These data suggest that an impairment of nitric oxide formation could be involved in the development of hypertension in this model.
本研究旨在检测正常血压和高血压糖尿病大鼠对一氧化氮合酶途径抑制和刺激的血压反应。与对照组相比,用链脲佐菌素(60mg/Kg腹腔注射)处理的大鼠出现高血糖、多尿和体重增加缓慢。一组糖尿病大鼠出现高血压,因此我们研究了三个实验组:对照大鼠(C)、正常血压糖尿病大鼠(ND)和高血压糖尿病大鼠(HD)。记录平均动脉压(MAP)、收缩压、舒张压和心率:基线时间、注射L-硝基精氨酸甲酯(L-NAME:1mg/Kg静脉注射)后30分钟以及注射L-精氨酸(L-arg:250mg/Kg静脉注射)后。L-NAME使所有组的MAP显著升高。糖尿病大鼠的这种升高幅度小于对照大鼠。HD组MAP的升高显著低于ND组。L-arg使所有组的MAP显著降低。与对照大鼠相比,糖尿病大鼠的这种降低显著减弱。糖尿病组中高血压大鼠对L-arg反应的低血压程度低于正常血压糖尿病大鼠。这些数据表明,一氧化氮生成受损可能参与了该模型中高血压的发生。