OBESITY-INDUCED HYPERTENSION - RENAL-FUNCTION AND SYSTEMIC HEMODYNAMICS
OBESITY-INDUCED HYPERTENSION - RENAL-FUNCTION AND SYSTEMIC HEMODYNAMICS
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DOI：
10.1161/01.hyp.22.3.292
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发表时间：
1993-09-01
期刊：
影响因子：
8.3
通讯作者：
SMITH, MJ
中科院分区：
文献类型：
--
作者：
HALL, JE;BRANDS, MW;SMITH, MJ
本研究探讨了控制肾脏血流动力学和肾小管功能，以及全身血流动力学，在肥胖引起的高血压在慢性仪器清醒的狗。平均动脉压，心输出量和心率监测，每天24小时使用计算机化的方法，水和电解质平衡每天测量，并在控制期间和5周的高脂饮食每周测量肾血流动力学。在7至10天的控制测量后，将0.5至0.9 kg的熟牛肉脂肪添加到常规饮食中，并且在整个研究期间将钠摄入量保持在76 mmol/d。高脂饮食5周后，体重从24.0 +/- 1.0增加到35.9 +/- 4.9 kg，平均动脉压从83 +/- 5增加到100 +/- 4 mm Hg，心输出量从2.86 +/- 0.27增加到4.45 +/- 0.55 L/min，心率从每分钟68 +/- 5上升到107 +/- 9。与高血压相关的是35天后累积钠平衡增加至507 +/- 107 mmol，碘酞酸钠空间（细胞外液体积指数）增加至对照组的131 +/- 4%。钠潴留是由于肾小管重吸收增加，因为肾小球滤过率和有效肾血浆流量在高脂饮食的5周内增加，在高脂饮食的第5周期间，平均分别为对照组的135 +/- 4%和149 +/- 19%。血浆肾素活性和血浆胰岛素浓度分别从0.46 +/- 0.12 ng血管紧张素I/mL/小时和11.1 +/- 2.6 muU/mL增加到1.10 +/- 0.23 ng血管紧张素I/mL/小时和30.1 +/- 7.0 muU/mL。由于尽管平均动脉压升高，但钠排泄减少，因此肥胖诱导的犬高血压与肾小管重吸收增加引起的肾压尿钠排泄转移有关，尽管发生这种情况的确切机制尚不清楚。
This study examined the control of renal hemodynamics and tubular function, as well as systemic hemodynamics, during obesity-induced hypertension in chronically instrumented conscious dogs. Mean arterial pressure, cardiac output, and heart rate were monitored 24 hours a day using computerized methods, water and electrolyte balances were measured daily, and renal hemodynamics were measured each week during the control period and 5 weeks of a high-fat diet. After 7 to 10 days of control measurements, 0.5 to 0.9 kg of cooked beef fat was added to the regular diet, and sodium intake was maintained constant at 76 mmol/d throughout the study. After 5 weeks of the high-fat diet, body weight increased from 24.0 +/- 1.0 to 35.9 +/- 4.9 kg, mean arterial pressure increased from 83 +/- 5 to 100 +/- 4 mm Hg, cardiac output increased from 2.86 +/- 0.27 to 4.45 +/- 0.55 L/min, and heart rate rose from 68 +/- 5 to 107 +/- 9 beats per minute. Associated with the hypertension was an increase in cumulative sodium balance to 507 +/- 107 mmol after 35 days and a rise in sodium iothalamate space, an index of extracellular fluid volume, to 131 +/- 4% of control. Sodium retention was due to increased tubular reabsorption, because glomerular filtration rate and effective renal plasma flow increased throughout the 5 weeks of the high-fat diet, averaging 135 +/- 4% and 149 +/- 19% of control, respectively, during the fifth week of the high-fat diet. Plasma renin activity and plasma insulin concentration increased from 0.46 +/- 0.12 ng angiotensin I/mL per hour and 11.1 +/- 2.6 muU/mL, respectively, to 1.10 +/- 0.23 ng angiotensin I/mL per hour and 30.1 +/- 7.0 muU/mL after 5 weeks. Because decreased sodium excretion occurred despite elevated mean arterial pressure, obesity-induced hypertension in dogs is associated with a shift of renal pressure natriuresis that is caused by increased tubular reabsorption, although the exact mechanism by which this occurs is still unclear.