Fregoneze J B, Luz C P, Sarmento C, Gonzalez V, Oliveira P, Santana P, Marinho C A, Castro L, Nascimento T, De Paula S, Lima A K, De Oliveira I R, De Castro-e-Silva E
Department of Zoology, Biology Institute, Federal University of Bahia, Salvador, Brazil.
Physiol Behav. 1998 Nov 15;65(2):321-6. doi: 10.1016/s0031-9384(98)00172-3.
The aim of the present experiments was to discern whether central acute lead injections affect brain control of renal function. Adult Wistar male rats received third-ventricle injections of lead acetate in three different doses (0.03, 0.3, and 3.0 nmol/rat). Lead acetate induced a significant increase in renal excretion of sodium and potassium. Pretreatment with losartan, a selective angiotensin II AT1 receptor antagonist (10.8 nmol/rat into the third ventricle 10 min before central lead injection), inhibits lead-induced natriuretic and kaliuretic effects. In addition, pretreatment with gadolinium, a calcium-channel blocker (0.3 nmol/rat into the third ventricle 20 min before central lead administration), reversed the increase in renal excretion of sodium and potassium provoked by central lead administration. Taken together, the data presented here suggest that lead injected into the third ventricle increases renal excretion of sodium and potassium by a mechanism that depends on the functional integrity of central angiotensin II AT1 receptors and calcium channels.
本实验的目的是探究中枢急性注射铅是否会影响大脑对肾功能的控制。成年雄性Wistar大鼠接受了三种不同剂量（0.03、0.3和3.0 nmol/只大鼠）的醋酸铅第三脑室注射。醋酸铅导致钠和钾的肾排泄显著增加。用氯沙坦（一种选择性血管紧张素II AT1受体拮抗剂，在中枢注射铅前10分钟向第三脑室注射10.8 nmol/只大鼠）进行预处理，可抑制铅诱导的利钠和利尿作用。此外，用钆（一种钙通道阻滞剂，在中枢给予铅前20分钟向第三脑室注射0.3 nmol/只大鼠）进行预处理，可逆转中枢给予铅所引起的钠和钾肾排泄增加。综上所述，此处呈现的数据表明，注入第三脑室的铅通过一种依赖于中枢血管紧张素II AT1受体和钙通道功能完整性的机制增加钠和钾的肾排泄。
