Hall J E, Coleman T G, Mizelle H L
Department of Physiology and Biophysics, University of Mississippi, Jackson 39216-4505.
Am J Hypertens. 1989 Mar;2(3 Pt 1):171-3. doi: 10.1093/ajh/2.3.171.
The aim of this study was to determine whether chronic hyperinsulinemia, comparable to that found in obesity-associated hypertension, causes sustained increases in mean arterial pressure (MAP) or potentiates the hypertensive effects of angiotensin II (ANG II). Insulin infusion (0.5 or 1.0 mU/kg/min, IV), with plasma glucose held constant by IV glucose infusion, for seven to 28 days raised plasma insulin by five- to ten-fold, but did not significantly change MAP in dogs with reduced kidney mass that were maintained on high sodium intake. In dogs infused with ANG II to cause mild hypertension, insulin for 28 days did not potentiate the hypertension. Insulin infusion did, however, cause modest sodium retention during the first few days of infusion. These findings suggest that additional factors besides hyperinsulinemia per se are responsible for obesity-associated hypertension.
本研究的目的是确定与肥胖相关高血压中发现的慢性高胰岛素血症是否会导致平均动脉压(MAP)持续升高,或增强血管紧张素II(ANG II)的高血压作用。通过静脉输注葡萄糖使血浆葡萄糖保持恒定,以0.5或1.0 mU/kg/分钟的速率静脉输注胰岛素7至28天,可使肾质量减少且高钠摄入的犬的血浆胰岛素升高5至10倍,但并未显著改变其MAP。在输注ANG II以引起轻度高血压的犬中,胰岛素输注28天并未增强高血压作用。然而,胰岛素输注在输注的最初几天确实会导致适度的钠潴留。这些发现表明,除了高胰岛素血症本身之外,其他因素也与肥胖相关高血压有关。