Fregoneze J B, Luz C P, Castro L, Oliveira P, Lima A K, Souza F, Maldonado I, Macêdo D F, Ferreira M G, Bandeira I P, Rocha M A, Carvalho F L, De-Castro-e-Silva E
Departamento de Zoologia, Instituto de Biologia, Universidade Federal da Bahia, Salvador, BA, Brasil.
Braz J Med Biol Res. 1999 Oct;32(10):1217-22. doi: 10.1590/s0100-879x1999001000007.
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 ss-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 ss-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.
我们已经证明，向脱水大鼠以及受到中枢胆碱能和血管紧张素能刺激的大鼠微量中枢注射锌会诱导显著的抗渴作用。在此我们表明，向Wistar大鼠（体重190 - 250克）第三脑室急性注射锌也会阻断中枢β - 肾上腺素能刺激诱导的饮水。纳洛酮对阿片类通路的中枢抑制可逆转脱水大鼠中锌诱导的抗渴作用。120分钟后，接受第三脑室注射异丙肾上腺素（160纳摩尔/只大鼠）的大鼠与接受生理盐水处理的对照组（0.15±0.07毫升/100克体重）相比，饮水量显著增加（5.78±0.54毫升/100克体重）。用锌预处理（3.0、30.0和300.0皮摩尔/只大鼠，在注射异丙肾上腺素前45分钟）以剂量依赖的方式阻断饮水。在所采用的最高剂量下，可证明完全阻断（0.54±0.2毫升/100克体重）。120分钟后，如预期的那样，对照（用醋酸钠处理）脱水大鼠饮水量很高（7.36±0.39毫升/100克体重）。中枢注射锌可阻断这种反应（2.5±0.77毫升/100克体重）。纳洛酮预处理（82.5纳摩尔/只大鼠，在注射锌前30分钟）使饮水量恢复到无锌脱水动物中观察到的高水平（7.04±0.56毫升/100克体重）。这些数据表明，锌能够阻断中枢β - 肾上腺素能刺激诱导的饮水，并且锌诱导的脱水大鼠饮水阻断可能至少部分归因于中枢阿片肽的刺激。
