Lopez-Sela P, Brime J I, Diaz F, Marin B, Costales M, Vijande M
Dpto. de Biología Funcional, Area de Fisiología, Universidad de Oviedo, Spain.
Appetite. 1989 Oct;13(2):143-54. doi: 10.1016/0195-6663(89)90111-6.
Male wistar rats drank in a dose-related manner, in response to 1 to 40 U/kg of i.p. insulin. Maximum intakes took place during the first 30 min after i.p. insulin administration, coinciding with the period of maximal drop of blood glucose. Plasma renin activity (PRA) in rats treated with i.p. insulin was higher than in basal conditions or after saline injection. Nephrectomy and adrenalectomy did not abolish insulin-induced drinking. A low dose of captopril (0.1 mg/kg s.c.) did not modify insulin-induced drinking, but a higher dose (10 mg/kg s.c.), or enalapril (0.5 mg/microgram s.c.), significantly increased insulin-induced drinking. Enhancement of insulin-induced drinking by s.c. captopril was not secondary to an increased diuresis. Captopril (50 micrograms i.c.v.) significantly reduced the cumulative water intake after i.p. insulin (20 U/kg i.p.) plus s.c. captopril (10 mg/kg). The blockade of central receptors for angiotensin II with sarile-AII (5 micrograms) significantly diminished insulin-induced drinking. It appears that the peripheral renin angiotensin system is not necessary for insulin-induced drinking but central angiotensin II plays an important role.
雄性Wistar大鼠对1至40 U/kg腹腔注射胰岛素呈剂量依赖性饮水。最大饮水量出现在腹腔注射胰岛素后的前30分钟内,这与血糖最大降幅的时间段一致。腹腔注射胰岛素的大鼠血浆肾素活性(PRA)高于基础状态或注射生理盐水后。肾切除术和肾上腺切除术并未消除胰岛素诱导的饮水。低剂量的卡托普利(0.1 mg/kg皮下注射)并未改变胰岛素诱导的饮水,但较高剂量(10 mg/kg皮下注射)或依那普利(0.5 mg/μg皮下注射)显著增加了胰岛素诱导的饮水。皮下注射卡托普利增强胰岛素诱导的饮水并非继发于利尿增加。卡托普利(50 μg脑室内注射)显著降低了腹腔注射胰岛素(20 U/kg腹腔注射)加皮下注射卡托普利(10 mg/kg)后的累积饮水量。用Sarile-AII(5 μg)阻断血管紧张素II的中枢受体可显著减少胰岛素诱导的饮水。似乎外周肾素-血管紧张素系统对于胰岛素诱导的饮水并非必需,但中枢血管紧张素II起重要作用。