de Arruda Camargo Luiz Antonio, Saad Wilson Abrão, Cerri Paulo Sérgio
Department of Physiology, School of Dentistry Paulista State University, UNESP, Rua Humaitá, 1680, Araraquara, SP 14801-903, Brazil.
Brain Res Bull. 2003 Sep 30;61(5):481-7. doi: 10.1016/s0361-9230(03)00184-9.
In this study, we investigated the influence of d(CH(2))(5)-Tyr (Me)-AVP (AAVP) an antagonist of V(1) receptors of arginine(8)-vasopressin (AVP) and the effects of losartan and CGP42112A (selective ligands of the AT(1) and AT(2) angiotensin receptors, respectively) injections into the paraventricular nucleus (PVN) on the thirst effects of AVP stimulation of the lateral septal area (LSA). AVP injection into the LSA increased the water intake in a dose-dependent manner. AAVP injected into the PVN produced a dose-dependent reduction of the drinking responses elicited by LSA administration of AVP. Both the AT(1) and AT(2) ligands administered into the PVN elicited a concentration-dependent inhibition in the water intake induced by AVP injected into the LSA, but losartan was more effective than CGP42112A the increase in the AVP response. These results indicate that LSA dipsogenic effects induced by AVP are mediated primarily by PVN AT(1) receptors. However, doses of losartan were more effective when combined with CGP42112A than when given alone, suggesting that the thirst induced by AVP injections into LSA may involve activation of multiple angiotensin II (ANG II) receptor subtypes. These results also suggests that facilitatory effects of AVP on water intake into the LSA are mediated through the activation of V(1)-receptors and that the inhibitory effect requires V(2)-receptors. Based on the present findings, we suggest that the administration of AVP into the LSA may play a role in the PVN control of water control.
在本研究中,我们调查了精氨酸加压素(AVP)V1受体拮抗剂d(CH(2))(5)-Tyr (Me)-AVP(AAVP)的影响,以及将氯沙坦和CGP42112A(分别为AT1和AT2血管紧张素受体的选择性配体)注射到室旁核(PVN)对AVP刺激外侧隔区(LSA)所产生的渴觉效应的影响。向LSA注射AVP会以剂量依赖性方式增加水摄入量。向PVN注射AAVP会使LSA给予AVP所引发的饮水反应产生剂量依赖性降低。向PVN注射AT1和AT2配体均会对向LSA注射AVP所诱导的水摄入量产生浓度依赖性抑制,但氯沙坦比CGP42112A对AVP反应增强的效果更显著。这些结果表明,AVP诱导的LSA致渴效应主要由PVN的AT1受体介导。然而,氯沙坦与CGP42112A联合使用时比单独使用更有效,这表明向LSA注射AVP所诱导的渴觉可能涉及多种血管紧张素II(ANG II)受体亚型的激活。这些结果还表明,AVP对LSA水摄入的促进作用是通过V1受体的激活介导的,而抑制作用则需要V2受体。基于目前的研究结果,我们认为向LSA注射AVP可能在PVN对水的控制中发挥作用。