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首页> 外文期刊>Kidney international. >Loss of glomerular responses to vasoconstrictor agents in rabbits recovering from ARF
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Loss of glomerular responses to vasoconstrictor agents in rabbits recovering from ARF

机译:从ARF中恢复的家兔肾小球对血管收缩药的反应丧失

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摘要

Loss of glomerular responses to vasoconstrictor agents in rabbits recovering from ARF. Glomerular responses to angiotensin II (All), arginine vasopressin (AVP), and norepinephrine (NE) were estimated in rabbits recovering from uranium–mediated nephropathy or ischemic acute renal failure (ARF) to examine roles of intraglomerular events in resistance to ARF. Uranyl acetate (UA, 0.8 mg/kg) produced ARF in some animals but did not in others. Rabbits recovering from UA-induced ARF were highly resistant to a rechallenge with a larger dose of the agent (2 mg/kg). Their glomeruli did not respond to AII, AVP and NE in vitro. In animals having not experienced ARF following the initial insult, however, resistance to the rechallenge was lower than in animals recovering from ARF, and the glomerular response to contractile stimuli was well sustained. A two hour clamping of the renal artery induced ARF in uninephrectomized rabbits. These animals were not resistant to an additional ischemia in the recovery phase, despite inhibited glomerular contractile response to AII. These data indicate a nonspecific inhibition of glomerular responses to contractile stimuli in the recovery phase of ARF. It is unlikely, however, that resistance to ARF can be attributed to the loss of the glomerular contractile response.
机译:从ARF恢复的兔子肾小球对血管收缩药的反应丧失。在从铀介导的肾病或缺血性急性肾衰竭(ARF)中恢复的兔子中,估计了其对血管紧张素II(全部),精氨酸加压素(AVP)和去甲肾上腺素(NE)的肾小球反应,以检查肾小球内事件对ARF抵抗的作用。乙酸铀酰(UA,0.8 mg / kg)在某些动物中产生ARF,而在另一些动物中则没有。从UA诱导的ARF中恢复的兔子对再挑战具有更高的抵抗力,需要使用更大剂量的药物(2 mg / kg)。他们的肾小球在体外对AII,AVP和NE无反应。然而,在最初受到伤害后未经历ARF的动物中,对再挑战的抵抗力比从ARF中恢复的动物低,并且肾小球对收缩刺激的反应得以良好维持。在未切除子宫的兔子中,将肾动脉钳制两个小时后会引起ARF。尽管抑制了肾小球对AII的收缩反应,但这些动物在恢复期对额外的局部缺血没有抵抗力。这些数据表明肾小球肾小球对ARF恢复期对收缩刺激的反应的非特异性抑制。但是,对ARF的抗药性不可能归因于肾小球收缩反应的丧失。

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