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首页> 外文期刊>American Journal of Physiology >Deficiency in angiotensin AT1a receptors prevents diabetes-induced hypertension.
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Deficiency in angiotensin AT1a receptors prevents diabetes-induced hypertension.

机译：血管紧张素AT1a受体的缺乏可预防糖尿病引起的高血压。

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摘要

The renin-angiotensin system has been implicated in the etiology of the cardiovascular complications of diabetes. Our studies extend these findings to show a specific role for angiotensin AT1a receptors in mediating diabetes-induced hypertension. Male angiotensin AT1a knockout (AT1aKO) and wild-type (AT1aWT) mice with arterial telemetric catheters were injected with streptozotocin (STZ; 150 mg/kg ip). The STZ dose was selected on the basis of a dose-response experiment in C57/BL mice. Blood glucose, water intake, body weight, blood pressure (BP), and heart rate (HR) were measured over a 2-wk period. Estimates of BP and HR variance (BPV and HRV) and their low- and high-frequency domains were also determined. STZ induced similar levels of hyperglycemia and polydypsia in the groups. Mean arterial pressure (MAP) was increased from 100 +/- 6 to 124 +/- 6 mmHg in diabetic AT1aWT. MAP was unchanged in AT1aKO (80 +/- 4 vs. 85 +/- 5 mmHg, basal vs. STZ). Treatment with an ACE inhibitor, captopril, produced a greater reduction in MAP (-18%) in diabetic AT1aWT than in AT1aKO (-3.4%). BPV was lower in AT1aKO (19 +/- 0.5 vs. 9 +/- 2 mmHg(2), AT1aWT vs. AT1aKO). Diabetes reduced BPV but only in AT1aWT (19 +/- 0.5 vs. 8 +/- 1 mmHg(2), basal vs. STZ). There were no changes in HR in either group. In AT1aKO, STZ increased HRV and its high-frequency domain with no changes seen in AT1aWT. Results document that ANG AT1a receptors are critical in diabetes-induced hypertension and in cardiac autonomic responses.
机译：肾素-血管紧张素系统与糖尿病的心血管并发症的病因有关。我们的研究扩展了这些发现，以显示血管紧张素AT1a受体在介导糖尿病诱发的高血压中具有特定作用。雄性血管紧张素AT1a基因敲除（AT1aKO）和野生型（AT1aWT）小鼠通过动脉遥测导管注射链脲佐菌素（STZ; 150 mg / kg ip）。根据C57 / BL小鼠的剂量反应实验选择STZ剂量。在2周内测量血糖，水摄入量，体重，血压（BP）和心率（HR）。还确定了BP和HR方差（BPV和HRV）及其低频和高频域的估计值。 STZ在各组中诱导了相似的高血糖和多发性增生。糖尿病AT1aWT中的平均动脉压（MAP）从100 +/- 6 mmHg增加到124 +/- 6 mmHg。在AT1aKO中MAP保持不变（80 +/- 4 vs. 85 +/- 5 mmHg，基础相对于STZ）。用ACE抑制剂卡托普利治疗，与AT1aKO（-3.4％）相比，糖尿病AT1aWT的MAP降低更大（-18％）。 BPV在AT1aKO中较低（19 +/- 0.5 vs. 9 +/- 2 mmHg（2），AT1aWT与AT1aKO）。糖尿病降低了BPV，但仅在AT1aWT中降低（19 +/- 0.5 vs.8 +/- 1 mmHg（2），基础vs.STZ）。两组的心率均无变化。在AT1aKO中，STZ增加了HRV及其高频域，而AT1aWT中未见变化。结果证明，ANG AT1a受体在糖尿病诱发的高血压和心脏自主神经反应中至关重要。

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