Maeda C Y, Fernandes T G, Lulhier F, Irigoyen M C
Departamento de Fisiologia, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brasil.
Braz J Med Biol Res. 1995 Apr;28(4):497-501.
Although an increased prevalence of hypertension is associated with insulin-dependent diabetes, little is known about the effect of streptozotocin (STZ) diabetes on arterial pressure (AP) regulation in rats. Changes in AP induced by STZ, as well as associated factors in blood pressure regulation such as baroreflex sensitivity, plasma renin activity (PRA), plasma glucose and insulin levels and endothelium participation, were studied in male Wistar rats weighing 287 +/- 10 g. The same seven conscious rats were used for all measurements before and after STZ diabetes. AP pulses were stored on a videotape recorder and processed by a data acquisition system. Baroreflex sensitivity was evaluated by measuring heart rate (HR) changes induced by AP variations produced by phenylephrine and sodium nitroprusside injection. The effect of inhibition of nitric oxide synthesis with NG-nitro-L-arginine methyl ester (L-NAME, 10 mg/kg i.v. bolus plus infusion at 20 mg kg-1 h-1) on AP was evaluated in another set of rats (6 normal and 5 submitted to STZ treatment). STZ induced hyperglycemia (306 +/- 19 mg/dl), a reduction in mean arterial pressure (MAP, from 116 +/- 5 to 101 +/- 4 mmHg) and no changes in HR (320 +/- 10 vs 298 +/- 14 bpm). The tachycardic response to arterial pressure decreases was impaired (-2.29 +/- 0.5 vs -4.5 +/- 0.7 bpm/mmHg, in control) while the bradycardic response to arterial pressure increases was unchanged. Pressure responsiveness to phenylephrine was impaired after STZ (3.78 +/- 0.4 vs 6.73 +/- 0.8 mmHg microU-1 ml-1, in control).(ABSTRACT TRUNCATED AT 250 WORDS)
虽然高血压患病率增加与胰岛素依赖型糖尿病相关,但关于链脲佐菌素(STZ)诱导的糖尿病对大鼠动脉压(AP)调节的影响知之甚少。在体重为287±10 g的雄性Wistar大鼠中,研究了STZ诱导的AP变化以及血压调节中的相关因素,如压力反射敏感性、血浆肾素活性(PRA)、血浆葡萄糖和胰岛素水平以及内皮参与情况。在STZ诱导糖尿病前后,对相同的7只清醒大鼠进行了所有测量。AP脉冲存储在磁带记录器上,并由数据采集系统进行处理。通过测量去氧肾上腺素和硝普钠注射引起的AP变化所诱发的心率(HR)变化来评估压力反射敏感性。在另一组大鼠(6只正常大鼠和5只接受STZ治疗的大鼠)中,评估了用NG-硝基-L-精氨酸甲酯(L-NAME,10 mg/kg静脉推注加20 mg·kg⁻¹·h⁻¹输注)抑制一氧化氮合成对AP的影响。STZ诱导高血糖(306±19 mg/dl),平均动脉压(MAP)降低(从116±5降至101±4 mmHg),HR无变化(320±10对298±14次/分钟)。对动脉压降低的心动过速反应受损(对照组为-4.5±0.7次/分钟/mmHg,糖尿病组为-2.29±0.5次/分钟/mmHg),而对动脉压升高的心动过缓反应未改变。STZ后对去氧肾上腺素的压力反应性受损(对照组为6.73±0.8 mmHg·μU⁻¹·ml⁻¹,糖尿病组为3.78±0.4 mmHg·μU⁻¹·ml⁻¹)。(摘要截断于250字)