Hydralazine as antihypertensive therapy in obesity-related hypertension.

Hydralazine as antihypertensive therapy in obesity-related hypertension.
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肼屈嗪作为肥胖相关高血压的抗高血压治疗。

DOI:
10.1038/sj.ijo.0802573
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发表时间:
2004
期刊:
International journal of obesity and related metabolic disorders : journal of the International Association for the Study of Obesity
影响因子:
--
通讯作者:
Cohen,JS
Cohen,JS
中科院分区:
--
文献类型:
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作者:
Carroll,JF;King,JW;Cohen,JS

文献摘要

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目的:目的有两个:(1)确定在肥胖发展过程中使用肼苯哒嗪作为抗高血压治疗是否加剧了肥胖相关的心脏加速和激素异常;(2)确定肥胖者中无高血压是否减轻了肥胖相关的血流动力学异常、心脏肥大和激素水平。设计:将雌性新西兰白色兔分为瘦对照组(n= 12)、瘦肼屈嗪治疗组(n= 9)、肥胖对照组(n= 11)和肥胖肼屈嗪治疗组(n= 8)。使用遥测技术测定治疗前平均血压(BP)和心率(HR)。治疗前BP保持在12周的肥胖症的发展使用肼屈嗪。MEASUREMENTS:慢性测量血压和心率;血浆/血容量;湿和干心室重量;身体脂肪/水;和激素的配置文件(血浆肾素活性,醛固酮,皮质醇,心钠素,肾上腺素,去甲肾上腺素)。相反,RAS在瘦肼苯哒嗪中被激活,如血浆醛固酮增加所示。在肥胖肼苯哒嗪高血压的情况下,并没有导致衰减的cardiacacceleration,心脏肥大,或intravascular volumes.CONCLUSIONS:肼苯哒嗪治疗肥胖兔并没有加剧肥胖相关的心血管和激素的变化。尽管血压得到控制,但肥胖肼苯哒嗪患者的心率加速和心脏肥大仍持续存在,表明肥胖对这些变量的影响与高血压无关。肼苯哒嗪对RAS激活的影响在瘦兔和肥胖兔中不同,表明肼苯哒嗪作为对照治疗在评价抗高血压药物中的全身作用可能因基础病理学而异。
OBJECTIVE: The objectives were two-fold:(1) determine whether the use of hydralazine as antihypertensive therapy during obesity development exacerbated obesity-related cardioacceleration and hormonal abnormalities;(2) determine whether the absence of hypertension in obesity attenuated obesity-related abnormalities in hemodynamics, cardiac hypertrophy, and hormonal profile.DESIGN: Female New Zealand White rabbits were divided into lean control (n= 12), lean hydralazine-treated (n= 9), obese control (n= 11), and obese hydralazine-treated (n= 8) groups. Pretreatment mean blood pressure (BP) and heart rate (HR) were determined using telemetry. Pretreatment BP was maintained during 12 weeks of obesity development using hydralazine.MEASUREMENTS: Chronically measured BP and HR; plasma/blood volume; wet and dry ventricular weights; body fat/water; and hormonal profile (plasma renin activity, aldosterone, cortisol, atrial natriuretic peptide, adrenaline, and noradrenaline).RESULTS: Hydralazine treatment in obese animals attenuated obesity-related renin–angiotensin system (RAS) activation. In contrast, RAS was activated in lean hydralazine, as indicated by increased plasma aldosterone. The absence of hypertension in obese hydralazine did not result in attenuation of cardioacceleration, cardiac hypertrophy, or intravascular volumes.CONCLUSIONS: Hydralazine treatment in obese rabbits did not exacerbate obesity-related cardiovascular and hormonal alterations. Cardioacceleration and cardiac hypertrophy persisted in obese hydralazine despite BP control, suggesting hypertension-independent effects of obesity on these variables. Hydralazine's effects on RAS activation differed in lean and obese rabbits, suggesting that the systemic effects of hydralazine as a control therapy in evaluation of antihypertensive medications may differ depending on the underlying pathology.