Ikeda T, Ochi H
Tottori University College of Medical Care Technology, Tottori University Faculty of Medicine, Yonago, Japan.
Life Sci. 1998;62(22):1999-2004. doi: 10.1016/s0024-3205(98)00171-4.
To elucidate whether and why glucose directly influences renin secretion, the effect of glucose on renin secretion was investigated in the rat. In an in vivo study, renin activity significantly (p<0.01) increased from the basal value of 7.6 +/- 1.4 to 14.2 +/- 3.2 ng Ang I/ml/hr (mean +/- SD) after intravenous glucose (1.0 g/kg, in 50% glucose solution ) injection. Propranolol (10.5 mg/kg) pretreatment partly abolished the increase in renin activity induced by glucose injection. In an in vitro study, the isolated kidneys of male Wistar rats (200-250 g) were perfused with a basal perfusing medium containing 5.5 mM glucose for 20 min, and then perfused with the medium containing 16.5 mM glucose, 27.5 mM glucose, 5.5 mM glucose + 22 mM mannitol, 27.5 mM glucose + 1 microM phentolamine, or 27.5 mM glucose + 1 microM propranolol for 10 min, respectively. Renin activity was significantly increased from a basal value of 8.1 +/- 4.5 to peak value of 17.9 +/- 3.0 ng Ang I/ml/hr (p<0.01) by 16.5 mM glucose, to 59.0 +/- 10.5 ng Ang I/ml/hr (p<0.005) by 27.5 mM glucose, and to 24.7 +/- 5.8 ng Ang I/ml/hr (p<0.01) by 5.5 mM glucose + 22 mM mannitol. The increase in renin activity in the kidney perfused with 27.5 mM glucose was significantly (p<0.005) higher than that with 16.5 mM glucose or that with 5.5 mM glucose + 22 mM mannitol. The 27.5 mM glucose-stimulated increase in renin activity was not changed by the addition of 1 microM phentolamine, while it was completely abolished by the addition of 1 microM propranolol. These results suggest that glucose has a direct stimulating effect on renin secretion probably through beta-adrenergic mechanisms in the rat.
为了阐明葡萄糖是否以及为何直接影响肾素分泌,在大鼠中研究了葡萄糖对肾素分泌的影响。在一项体内研究中,静脉注射葡萄糖(1.0 g/kg,溶于50%葡萄糖溶液)后,肾素活性从基础值7.6±1.4显著(p<0.01)增加至14.2±3.2 ng血管紧张素I/ml/小时(平均值±标准差)。普萘洛尔(10.5 mg/kg)预处理部分消除了葡萄糖注射诱导的肾素活性增加。在一项体外研究中,将雄性Wistar大鼠(200 - 250 g)的离体肾脏先用含5.5 mM葡萄糖的基础灌注培养基灌注20分钟,然后分别用含16.5 mM葡萄糖、27.5 mM葡萄糖、5.5 mM葡萄糖 + 22 mM甘露醇、27.5 mM葡萄糖 + 1 μM酚妥拉明或27.5 mM葡萄糖 + 1 μM普萘洛尔的培养基灌注10分钟。肾素活性因16.5 mM葡萄糖从基础值8.1±4.5显著增加至峰值17.9±3.0 ng血管紧张素I/ml/小时(p<0.01),因27.5 mM葡萄糖增加至59.0±10.5 ng血管紧张素I/ml/小时(p<0.005),因5.5 mM葡萄糖 + 22 mM甘露醇增加至24.7±5.8 ng血管紧张素I/ml/小时(p<0.01)。用27.5 mM葡萄糖灌注的肾脏中肾素活性的增加显著(p<0.005)高于用16.5 mM葡萄糖或5.5 mM葡萄糖 + 22 mM甘露醇灌注的情况。添加1 μM酚妥拉明未改变27.5 mM葡萄糖刺激的肾素活性增加,而添加1 μM普萘洛尔则完全消除了这种增加。这些结果表明,在大鼠中葡萄糖可能通过β - 肾上腺素能机制对肾素分泌有直接刺激作用。