Menani J V, Barbosa S P, McKinley M J, Wade J D, De Luca L A
Department of Physiology and Pathology, School of Dentistry, Paulista State University, 14801-903 Araraquara, São Paulo, Brazil.
Brain Res. 2004 Dec 24;1030(1):74-80. doi: 10.1016/j.brainres.2004.09.048.
It has been shown that central or peripheral injections of the peptide relaxin induces water intake, not sodium intake in rats. Important inhibitory mechanisms involving serotonin and other neurotransmitters in the control of water and NaCl intake have been demonstrated in the lateral parabrachial nucleus (LPBN). In the present study, we investigated the effects of bilateral injections of methysergide (serotonergic receptor antagonist) into the LPBN on intracerebroventricular (i.c.v.) relaxin-induced water and NaCl intake in rats. Additionally, the effect of the blockade of central angiotensin AT(1) receptors with i.c.v. losartan on relaxin-induced water and NaCl intake in rats treated with methysergide into the LPBN was also investigated. Male Holtzman rats with cannulas implanted into the lateral ventricle (LV) and bilaterally in the LPBN were used. Intracerebroventricular injections of relaxin (500 ng/1 microl) induced water intake (5.1+/-0.7 ml/120 min), but not significant 1.8% NaCl intake (0.5+/-0.4 ml/120 min). Bilateral injections of methysergide (4 microg/0.2 microl) into the LPBN strongly stimulated relaxin-induced 1.8% NaCl intake (34.5+/-10.9 ml/120 min) and slightly increased water intake (10.5+/-4.9 ml/120 min). The pretreatment with i.c.v. losartan (100 microg/1 microl) abolished the effects of i.c.v. relaxin combined with LPBN methysergide on 1.8% NaCl intake (0.5+/-0.4 ml/120 min). Losartan (100 microg/1 microl) also abolished relaxin-induced water intake in rats injected with methysergide into the LPBN (1.6+/-0.8 ml/120 min) or not (0.5+/-0.3 ml/120 min). Losartan (50 microg/1 microl) partially reduced the effects of relaxin. The results show that central relaxin interacting with central angiotensinergic mechanisms induces NaCl intake after the blockade of LPBN serotonergic mechanisms.
研究表明，向大鼠中枢或外周注射肽类松弛素会促使其饮水，而非摄取钠。业已证明，在外侧臂旁核（LPBN）中，涉及血清素及其他神经递质的重要抑制机制在水和氯化钠摄取的控制中发挥作用。在本研究中，我们探究了向LPBN双侧注射麦角新碱（血清素能受体拮抗剂）对大鼠脑室内（i.c.v.）注射松弛素所诱导的水和氯化钠摄取的影响。此外，还研究了用i.c.v.氯沙坦阻断中枢血管紧张素AT(1)受体对向LPBN注射麦角新碱的大鼠松弛素诱导的水和氯化钠摄取的影响。使用了在侧脑室（LV）及双侧LPBN植入套管的雄性霍尔兹曼大鼠。脑室内注射松弛素（500纳克/1微升）可诱导饮水（5.1±0.7毫升/120分钟），但对1.8%氯化钠的摄取不显著（0.5±0.4毫升/120分钟）。向LPBN双侧注射麦角新碱（4微克/0.2微升）强烈刺激了松弛素诱导的1.8%氯化钠摄取（34.5±10.9毫升/120分钟），并使饮水量略有增加（10.5±4.9毫升/120分钟）。i.c.v.氯沙坦（100微克/1微升）预处理消除了i.c.v.松弛素联合LPBN麦角新碱对1.8%氯化钠摄取的影响（0.5±0.4毫升/120分钟）。氯沙坦（100微克/1微升）也消除了向LPBN注射麦角新碱或未注射麦角新碱的大鼠中松弛素诱导的饮水（分别为1.6±0.8毫升/120分钟和0.5±0.3毫升/120分钟）。氯沙坦（50微克/1微升）部分降低了松弛素的作用。结果表明，在阻断LPBN血清素能机制后，中枢松弛素与中枢血管紧张素能机制相互作用会诱导氯化钠摄取。
