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首页> 外文期刊>Methods and findings in experimental and clinical pharmacology >Clonidine and a novel clonidine analog AL-12 cause sympathoinhibition in spontaneously hypertensive and diabetic spontaneously hypertensive rats.
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Clonidine and a novel clonidine analog AL-12 cause sympathoinhibition in spontaneously hypertensive and diabetic spontaneously hypertensive rats.

机译：可乐定和新型可乐定类似物AL-12在自发性高血压和糖尿病自发性高血压大鼠中引起交感神经抑制。

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This study examined the sympathoinhibitory effects of clonidine and a novel clonidine analog, AL-12, in rat models of genetic hypertension and a combined state of genetic hypertension and diabetes. Rats in the treatment groups were given either clonidine or AL-12 while the respective control groups received either saline or Tween 80 for 6 days. Physiological data were collected during this period, which was followed by acute studies on day 7 when bolus administrations (i.v.) of graded doses of noradrenaline, phenylephrine and methoxamine were carried out. It was observed that in AL-12-treated nondiabetic spontaneously hypertensive rats (SHR), the pressure responses to all adrenergic agonists were greater (p < 0.05) in the treated group, while in the diabetic SHR rats a larger pressure response was observed only to noradrenaline (p < 0.05). In nondiabetic SHR rats treated with clonidine, a greater (p < 0.05) pressure response was observed only in the case of phenylephrine. In the diabetic SHR rats treated with clonidine, the pressure responses to the adrenergic agonists were similar (p > 0.05) in the treated and its control animals except that methoxamine caused a greater (p < 0.05) pressure response in the control group. The data obtained suggest that clonidine and AL-12 act possibly via vascular alpha1 and alpha2 adrenoceptors present at both pre- and postsynaptic locations.
机译：这项研究检查了可乐定和新型可乐定类似物AL-12在遗传性高血压以及遗传性高血压和糖尿病合并状态的模型中的交感神经抑制作用。给治疗组的大鼠服用可乐定或AL-12，而各对照组则接受生理盐水或吐温80的治疗，持续6天。在此期间收集了生理数据，随后在第7天进行了急性研究，当时进行了大剂量的去甲肾上腺素，去氧肾上腺素和甲氧胺的推注（i.v.）。观察到，在AL-12治疗的非糖尿病自发性高血压大鼠（SHR）中，治疗组对所有肾上腺素能激动剂的压力反应均较大（p <0.05），而在糖尿病SHR大鼠中，仅观察到较大的压力反应去甲肾上腺素（p <0.05）。在用可乐定治疗的非糖尿病SHR大鼠中，仅在去氧肾上腺素的情况下观察到更大的压力响应（p <0.05）。在用可乐定治疗的糖尿病SHR大鼠中，在治疗组及其对照组动物中，对肾上腺素能激动剂的压力反应相似（p> 0.05），只是在对照组中甲氧胺引起更大的压力反应（p <0.05）。获得的数据表明可乐定和AL-12可能通过突触前和突触后位置均存在的血管α1和α2肾上腺素受体起作用。

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