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首页> 外文期刊>Hypertension: An Official Journal of the American Heart Association >Pathogenesis of hypertension in the sinoaortic-denervated spontaneously hypertensive rat.
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Pathogenesis of hypertension in the sinoaortic-denervated spontaneously hypertensive rat.

机译:自发性高血压的大鼠主动脉高血压的发病机理。

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The present study was performed to examine the relation between the gain of the baroreceptor reflex and the pathogenesis of hypertension in the spontaneously hypertensive rat. Spontaneously hypertensive or Wistar-Kyoto rats underwent either sinoaortic baroreceptor denervation or sham denervation at 28-35 days of age. Four months later these rats were chronically instrumented for measurements of arterial pressure and heart rate. Sixty-minute computerized measurements of arterial pressure showed no difference between spontaneously hypertensive sham (163 +/- 5 mm Hg) and spontaneously hypertensive baroreceptor-denervated (166 +/- 5 mm Hg) rats, or Wistar-Kyoto sham (114 +/- 3 mm Hg) and Wistar-Kyoto baroreceptor-denervated (121 +/- 4 mm Hg) rats. The gain of baroreceptor reflex control of heart rate was assessed by measuring maximal heart rate responses to changes in arterial pressure elicited by bolus injection of phenylephrine and nitroprusside (gain = slope of linear regression equation of change in heart rate versus change in arterial pressure). Baroreceptor reflex gain was significantly higher in Wistar-Kyoto sham rats (-2.10 beats/min/mm Hg) than spontaneously hypertensive sham rats (-0.94 beats/min/mm Hg). Baroreceptor denervation significantly decreased baroreceptor reflex gain in both Wistar-Kyoto (-0.26 mm Hg) and spontaneously hypertensive (-0.22 beats/min/mm Hg) groups. Since baroreceptor denervation did not exacerbate the development of hypertension in adult spontaneously hypertensive rats or lead to hypertension in Wistar-Kyoto rats, we conclude that a primary dysfunction in the baroreceptor reflex alone is not responsible for the development of hypertension in this model.
机译:本研究旨在检查自发性高血压大鼠压力感受器反射的获得与高血压的发病机制之间的关系。自发性高血压或Wistar-Kyoto大鼠在28-35天时经历了鼻窦压力感受器神经支配或假神经支配。四个月后,这些大鼠被长期用于测量动脉压和心率。 60分钟计算机化的动脉压测量显示,自发性高血压假手术(163 +/- 5 mm Hg)和自发性高血压压力感受器去神经(166 +/- 5 mm Hg)大鼠或Wistar-Kyoto假手术(114 + / -3毫米汞柱)和Wistar-Kyoto压力感受器去神经支配(121 +/- 4毫米汞柱)大鼠。通过测量快速推注苯肾上腺素和硝普钠引起的动脉压变化的最大心率响应来评估心率压力感受器反射控制的增益(增益=心率变化与动脉压变化的线性回归方程的斜率)。 Wistar-Kyoto假手术大鼠的压力感受器反射增益显着高于自发性高血压假手术大鼠(-2.10次/分钟/ mm Hg)。 Wistar-Kyoto(-0.26 mm Hg)和自发性高血压(-0.22 beats / min / mm Hg)组的压力感受器去神经支配显着降低了压力感受器反射增益。由于压力感受器去神经支配并不会加剧成年自发性高血压大鼠的高血压发展或在Wistar-Kyoto大鼠中导致高血压,因此我们得出结论,在该模型中,仅压力感受器反射的主要功能障碍与高血压的发展无关。

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