de Oliveira Lisandra Brandino, De Luca Laurival Antonio, Menani José Vanderlei
Department of Physiology and Pathology, School of Dentistry, Paulista State University, UNESP, Rua Humaitá, 1680 Araraquara, SP, Brazil.
Brain Res. 2003 Dec 12;993(1-2):177-82. doi: 10.1016/j.brainres.2003.09.011.
Central injections of the alpha(2) adrenergic/imidazoline receptor agonist moxonidine inhibit water and NaCl intake in rats. In the present study, we investigated the possible involvement of central alpha(2) adrenergic receptors on the inhibitory effect of moxonidine in 0.3 M NaCl intake induced by 24 h sodium depletion. Male Holtzman rats with stainless-steel cannulas implanted into the lateral ventricle (LV) were used. Sodium depletion was produced by the treatment with the diuretic furosemide (20 mg/kg of body weight) injected subcutaneously +24 h of sodium-deficient diet. Intracerebroventricular (icv) injections of moxonidine (20 nmol/1 microl) reduced sodium depletion-induced 0.3 M NaCl intake (6.6+/-1.9 ml/120 min vs. vehicle: 12.7+/-1.7 ml/120 min). Pre-treatment with the alpha(2) adrenoreceptor antagonists RX 821002 (80 nmol/1 microl), SK&F 86466 (640 nmol/1 microl) and yohimbine (320 nmol/3 microl) injected icv abolished the inhibitory effect of icv moxonidine on sodium depletion-induced 0.3 M NaCl intake (13.3+/-1.4, 15.7+/-1.7 and 11.8+/-2.2 ml/120 min, respectively). The results show that the activation of alpha(2) adrenoreceptors is essential for the inhibitory effect of central moxonidine on sodium depletion-induced NaCl intake.
向大鼠脑室内注射α₂肾上腺素能/咪唑啉受体激动剂莫索尼定可抑制水和氯化钠的摄入。在本研究中,我们调查了中枢α₂肾上腺素能受体是否可能参与莫索尼定对24小时钠缺乏诱导的0.3M氯化钠摄入的抑制作用。使用植入侧脑室(LV)的不锈钢套管的雄性霍尔茨曼大鼠。通过皮下注射利尿剂呋塞米(20mg/kg体重)+24小时缺钠饮食来产生钠缺乏。脑室内(icv)注射莫索尼定(20nmol/1μl)可减少钠缺乏诱导的0.3M氯化钠摄入(6.6±1.9ml/120分钟,而溶剂对照组为:12.7±1.7ml/120分钟)。预先通过脑室内注射α₂肾上腺素能受体拮抗剂RX 821002(80nmol/1μl)、SK&F 86466(640nmol/1μl)和育亨宾(320nmol/3μl)可消除脑室内注射莫索尼定对钠缺乏诱导的0.3M氯化钠摄入的抑制作用(分别为13.3±1.4、15.7±1.7和11.8±2.2ml/120分钟)。结果表明,α₂肾上腺素能受体的激活对于中枢莫索尼定对钠缺乏诱导的氯化钠摄入的抑制作用至关重要。