Saad W A, Camargo L A, Renzi A, de Luca Júnior L A, Antunes-Rodrigues J, Saad W A
Department of Physiology, School of Dentistry, Paulista State University, Araraquara, SP, Brazil.
Neurosci Lett. 1992 Jan 6;134(2):212-4. doi: 10.1016/0304-3940(92)90519-d.
In the present study we investigated the effects of central (i.c.v.) and subcutaneous (s.c.) injections of a 2 micrograms dose of lisinopryl, an inhibitor of angiotensin I(ANGI)-converting enzyme (CE), on water intake. I.c.v. but not s.c. injection of lisinopryl abolished drinking in response to s.c. isoprenaline (100 micrograms/kg) and significantly reduced drinking in response to 24 h water deprivation or s.c. polyethylene glycol (30% w/v, 10 ml/kg). Lisinopryl had no effect on water intake induced by cellular dehydration (s.c. injection of hypertonic saline (2 M NaCl)). These results are consistent with the hypothesis that lisinopryl acts as a CE blocking agent in the brain. The thrist challenge induced by hypotension using isoprenaline acts primarily by generating ANGII systemically and centrally. The other thirst challenges such as cellular dehydration are independent of the ANGII in the brain. This conclusion was made possible by utilizing a new CE blocking agent at a smaller dose than normally used for other ANG I-CE inhibitors.
在本研究中，我们研究了向脑室内（i.c.v.）和皮下（s.c.）注射2微克剂量的赖诺普利（一种血管紧张素I（ANGI）转换酶（CE）抑制剂）对水摄入的影响。脑室内注射赖诺普利可消除皮下注射异丙肾上腺素（100微克/千克）引起的饮水，并且显著减少24小时禁水或皮下注射聚乙二醇（30% w/v，10毫升/千克）引起的饮水。赖诺普利对细胞脱水（皮下注射高渗盐水（2M NaCl））诱导的水摄入没有影响。这些结果与赖诺普利在脑中作为CE阻断剂起作用的假设一致。使用异丙肾上腺素引起的低血压所诱导的口渴挑战主要通过在全身和中枢产生ANGII起作用。其他口渴挑战，如细胞脱水，与脑中的ANGII无关。通过使用一种新的CE阻断剂，且剂量比通常用于其他ANG I-CE抑制剂的剂量小，才得出了这一结论。
