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葡萄糖通过肾上腺素能机制刺激大鼠的肾素分泌。

Glucose stimulates renin secretion via adrenergic mechanisms in the rat.

作者信息

Ikeda T, Ochi H

机构信息

Tottori University College of Medical Care Technology, Tottori University Faculty of Medicine, Yonago, Japan.

出版信息

Life Sci. 1998;62(22):1999-2004. doi: 10.1016/s0024-3205(98)00171-4.

Abstract

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.

摘要

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。

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