Direct measurement of renal sympathetic nervous activity in high-fat diet-related hypertensive rats

被引:45
作者
Iwashita, S
Tanida, M
Terui, N
Ootsuka, Y
Shu, M
Kang, D
Suzuki, M [1 ]
机构
[1] Univ Tsukuba, Lab Exercise & Nutr, Inst Hlth & Sport Sci, Tsukuba, Ibaraki 3058574, Japan
[2] Univ Tsukuba, Inst Basic Med Sci, Tsukuba, Ibaraki 3058574, Japan
关键词
renal sympathetic nervous activity; blood pressure elevation; urine sodium excretion rate; high-fat diet; rat;
D O I
10.1016/S0024-3205(02)01707-1
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
The elevation of renal sympathetic nervous activity (SNA) is a possible cause of blood pressure (BP) elevation. Although a high-fat diet (FAT) often induces BP elevation in animals, the effect of FAT on renal SNA in animals is not consistent between studies. Thus, we compared the basal levels of efferent renal SNA and BP in FAT- or high-carbohydrate diet (CHO)-fed rats. Twenty-four male Sprague-Dawley rats were fed FAT (P/F/C=20/45/35% cal) or CHO (20/5/75) from 5 weeks of age. After 20-21 weeks of feeding, a 24-h urine sample was collected to measure sodium excretion. The next day, blood (0.2 ml) was withdrawn from a femoral artery, and basal efferent renal nerve discharges and mean arterial pressure (MAP) were recorded under anesthesia. Immediately after the experiment, abdominal (epididymal, perirenal and mesenteric) adipose tissues were dissected. Total abdominal fat weight was significantly greater in the FAT group than in the CHO group. The plasma level of leptin was significantly higher in the FAT group, but blood glucose and plasma insulin levels did not differ between the two groups. MAP and renal SNA were significantly higher in the FAT group. In addition, the ratio of urinary sodium excretion to dietary sodium intake was significantly lower in the FAT group than in the CHO group. The data suggest that the increased renal SNA may contribute to BP elevation in FAT-fed rats. The present study firstly demonstrated that renal SNA was elevated with FAT-related BP elevation. (C) 2002 Elsevier Science Inc. All rights reserved.
引用
收藏
页码:537 / 546
页数:10
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