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正常血压和自发性高血压大鼠中盐负荷对压力反射的差异性中枢调节

Differential central modulation of the baroreflex by salt loading in normotensive and spontaneously hypertensive rats.

作者信息

Ono A, Kuwaki T, Kumada M, Fujita T

机构信息

Fourth Department of Internal Medicine, The University of Tokyo, Japan.

出版信息

Hypertension. 1997 Mar;29(3):808-14. doi: 10.1161/01.hyp.29.3.808.

Abstract

In salt-sensitive hypertensive animal models and human subjects compared with their salt-resistant counterparts, sympathetic activity is abnormally enhanced during a high salt diet. We examined whether salt loading differentially modulates the arterial baroreceptor reflex (ABR), a major control mechanism of arterial pressure and sympathetic vasomotor activity, in young normotensive Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR). Six-week-old WKY and SHR were fed a normal (0.66%) or high (8.00%) salt diet for 4 weeks. After the diet regimen, baseline levels of mean arterial pressure (MAP), renal sympathetic nerve activity (RSNA), and the overall and central properties of the ABR were compared among the four groups of rats under halothane anesthesia. In WKY, a high salt diet did not affect baseline arterial pressure and RSNA but potentiated the ABR, as evidenced by an increase in the maximal slope of MAP-RSNA and MAP-heart rate relationships. In SHR, by contrast, salt loading accelerated hypertension and sympathetic overactivity and impaired the ABR. Salt-induced modulation of the ABR was associated with that of the central property, since reflex inhibition of RSNA by stimulation of the aortic depressor nerve was augmented in WKY and attenuated in SHR. These results suggest that differential modulation of the central mechanism subserving the baroreflex control of sympathetic activity at least partly accounts for the difference in salt sensitivity between WKY and SHR.

摘要

与盐抵抗性动物模型和人类受试者相比,盐敏感性高血压动物模型和人类受试者在高盐饮食期间交感神经活动异常增强。我们研究了在年轻的血压正常的Wistar-Kyoto大鼠(WKY)和自发性高血压大鼠(SHR)中,盐负荷是否以不同方式调节动脉压力感受器反射(ABR),这是动脉血压和交感神经血管运动活动的主要控制机制。六周龄的WKY和SHR被给予正常(0.66%)或高(8.00%)盐饮食4周。在饮食方案结束后,在氟烷麻醉下比较四组大鼠的平均动脉压(MAP)、肾交感神经活动(RSNA)的基线水平以及ABR的整体和中枢特性。在WKY中,高盐饮食不影响基线动脉血压和RSNA,但增强了ABR,MAP-RSNA和MAP-心率关系的最大斜率增加证明了这一点。相比之下,在SHR中,盐负荷加速了高血压和交感神经活动亢进,并损害了ABR。盐诱导的ABR调节与中枢特性的调节相关,因为刺激主动脉减压神经对RSNA的反射性抑制在WKY中增强而在SHR中减弱。这些结果表明,服务于交感神经活动压力反射控制的中枢机制的差异调节至少部分解释了WKY和SHR之间盐敏感性的差异。

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