首页> 外文期刊>Journal of biomedical science. >High sugar intake via the renin-angiotensin system blunts the baroreceptor reflex in adult rats that were perinatally depleted of taurine
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High sugar intake via the renin-angiotensin system blunts the baroreceptor reflex in adult rats that were perinatally depleted of taurine

机译:通过肾素-血管紧张素系统高糖摄入会抑制成年大鼠牛磺酸缺乏的成年大鼠的压力感受器反射

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Perinatal taurine depletion leads to several physiological impairments in adult life, in part, due to taurine’s effects on the renin-angiotensin system, a crucial regulator of growth and differentiation during early life. The present study tests the hypothesis that perinatal taurine depletion predisposes adult female rats to impaired baroreceptor control of arterial pressure by altering the renin-angiotensin system. Female Sprague Dawley (SD) rats were fed normal rat chow and from conception to weaning drank 3% beta-alanine in water (taurine depletion, TD) or water alone (Control, C). Female offspring ate a normal rat chow and drank water with (G) or without (W) 5% glucose throughout the experiment. To test the possible role of the renin-angiotensin system, 50% of the rats received captopril (an angiotensin converting enzyme inhibitor, 400 mg/L) from 7 days before parameter measurements until the end of experiment. At 7-8 weeks of age, arterial pressure, heart rate, baroreflex control of heart rate and renal nerve activity were studied in either conscious, freely moving or anesthetized rats. Perinatal taurine depletion did not alter resting mean arterial pressure or heart rate in the adult female offspring that received either high or normal sugar intake. Captopril treatment slightly decreased mean arterial pressure but not heart rate in all groups. Compared to controls, only the TDG rats displayed blunted baroreflex responses. Captopril treatment normalized baroreflex sensitivity in TDG. The present data indicate that in perinatal taurine depleted female rats, the renin-angiotensin system underlines the ability of high sugar intake to blunt baroreceptor responses.
机译:围产期牛磺酸的消耗会导致成年后的几种生理损伤,部分是由于牛磺酸对肾素-血管紧张素系统的影响,肾素-血管紧张素系统是生命早期生长和分化的重要调节剂。本研究检验了围产期牛磺酸耗竭使成年雌性大鼠通过改变肾素-血管紧张素系统而使动脉压力的压力感受器控制受损的假设。给雌性Sprague Dawley(SD)大鼠喂食正常的大鼠食物,从受孕到断奶时在水中(牛磺酸消耗,TD)或仅在水中(对照组,C)喝3%β-丙氨酸。在整个实验过程中,雌性后代吃了正常的大鼠食物,喝了(G)或不使用(W)5%的葡萄糖。为了测试肾素-血管紧张素系统的可能作用,从参数测量前7天到实验结束,有50%的大鼠接受了卡托普利(一种血管紧张素转化酶抑制剂,400 mg / L)。在7-8周龄时,在有意识,自由活动或麻醉的大鼠中研究了动脉压,心率,心律的压力反射控制和肾神经活动。围产期牛磺酸的消耗不会改变接受高糖或正常糖摄入量的成年雌性后代的静息平均动脉压或心率。卡托普利治疗在所有组中均使平均动脉压略有降低,但未降低心率。与对照组相比,只有TDG大鼠显示钝性压力反射反应。卡托普利治疗使TDG中的压力感受器反射敏感性标准化。目前的数据表明,在围产期牛磺酸耗尽的雌性大鼠中,肾素-血管紧张素系统强调了高糖摄入能钝化压力感受器反应的能力。

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