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Zinc and water intake in rats: investigation of adrenergic and opiatergic central mechanisms

机译:大鼠锌和水的摄入:肾上腺素能和鸦片中枢机制的研究

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We have demonstrated that central administration of zinc in minute amounts induces a significant antidipsogenic action in dehydrated rats as well as in rats under central cholinergic and angiotensinergic stimulation. Here we show that acute third ventricle injections of zinc also block water intake induced by central ?-adrenergic stimulation in Wistar rats (190-250 g). Central inhibition of opioid pathways by naloxone reverses the zinc-induced antidipsogenic effect in dehydrated rats. After 120 min, rats receiving third ventricle injections of isoproterenol (160 nmol/rat) exhibited a significant increase in water intake (5.78 ± 0.54 ml/100 g body weight) compared to saline-treated controls (0.15 ± 0.07 ml/100 g body weight). Pretreatment with zinc (3.0, 30.0 and 300.0 pmol/rat, 45 min before isoproterenol injection) blocked water intake in a dose-dependent way. At the highest dose employed a complete blockade was demonstrable (0.54 ± 0.2 ml/100 g body weight). After 120 min, control (NaAc-treated) dehydrated rats, as expected, exhibited a high water intake (7.36 ± 0.39 ml/100 g body weight). Central administration of zinc blocked this response (2.5 ± 0.77 ml/100 g body weight). Naloxone pretreatment (82.5 nmol/rat, 30 min before zinc administration) reverted the water intake to the high levels observed in zinc-free dehydrated animals (7.04 ± 0.56 ml/100 g body weight). These data indicate that zinc is able to block water intake induced by central ?-adrenergic stimulation and that zinc-induced blockade of water intake in dehydrated rats may be, at least in part, due to stimulation of central opioid peptides.
机译:我们已经证明,微量施用锌可在脱水大鼠以及在中央胆碱能和血管紧张素能刺激下的大鼠中诱导显着的抗双歧作用。在这里,我们显示了在Wistar大鼠(190-250克)中,急性第三脑室注射锌还会阻断中枢β-肾上腺素能刺激诱导的水摄入。纳洛酮对阿片样物质途径的中枢抑制作用可逆转脱水大鼠中锌诱导的抗成药作用。 120分钟后,与盐水处理对照组(0.15±0.07 ml / 100 g身体)相比,接受第三次心室注射异丙肾上腺素(160 nmol /大鼠)的大鼠水摄入量显着增加(5.78±0.54 ml / 100 g体重)。重量)。锌的预处理(异丙肾上腺素注射前45分钟,分别为3.0、30.0和300.0 pmol /大鼠)阻止了水的摄入,其剂量依赖性。在最高剂量下,可以证明完全阻断(0.54±0.2 ml / 100 g体重)。 120分钟后,对照组(经NaAc处理)脱水的大鼠,正如预期的那样,表现出较高的饮水量(7.36±0.39 ml / 100 g体重)。锌的中枢给药阻止了这种反应(2.5±0.77 ml / 100 g体重)。纳洛酮预处理(82.5 nmol /大鼠,施用锌前30分钟)将水摄入量恢复为无锌脱水动物中观察到的高水平(7.04±0.56 ml / 100 g体重)。这些数据表明锌能够阻断由中枢β-肾上腺素能刺激诱导的水摄取,并且锌诱导的对脱水大鼠中水摄取的阻断可能至少部分是由于对中央阿片样物质肽的刺激。

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