Gordon F J, Mark A L
Circ Res. 1984 Apr;54(4):378-87. doi: 10.1161/01.res.54.4.378.
Dahl salt-sensitive rats fed a low salt diet demonstrate functional impairment in baroreflex control of cardiovascular function prior to the development of hypertension. The purpose of this study was to identify the mechanism(s) responsible for impaired baroreflex control in prehypertensive Dahl salt-sensitive rats. To examine the central and efferent portions of the baroreflex arc, we electrically stimulated the aortic depressor nerve of urethane anesthetized Dahl salt-sensitive and Dahl salt-resistant rats while recording arterial pressure, heart rate, and sympathetic nerve activity. Aortic nerve stimulation produced equivalent responses in both groups, indicating that central and efferent mechanisms could not account for functional baroreflex impairment. In separate groups of Dahl rats, multifiber afferent aortic baroreceptor discharge was recorded while arterial pressure was increased with phenylephrine. Prehypertensive Dahl salt-sensitive rats demonstrated significantly less baroreceptor activation than Dahl salt-resistant rats, indicating that impaired baroreceptor discharge is the mechanism responsible for baroreflex abnormalities. Aortic arch distensibility was not different between Dahl strains, suggesting that impaired baroreceptor discharge in Dahl salt-sensitive rats is probably not due to abnormalities in vessel wall distensibility. Since arterial pressure of both Dahl strains was in the normotensive range and did not differ significantly between Dahl salt-sensitive and salt-resistant rats, baroreceptor impairment appears to be a primary defect in Dahl salt-sensitive rats, rather than being secondary to hypertension. We speculate that this impairment in baroreceptor function in Dahl salt-sensitive rats prior to any elevation in arterial pressure may contribute to the Dahl salt-sensitive rat's genetic propensity to develop hypertension.
喂食低盐饮食的 Dahl 盐敏感大鼠在高血压发展之前就表现出压力反射对心血管功能控制的功能损害。本研究的目的是确定导致高血压前期 Dahl 盐敏感大鼠压力反射控制受损的机制。为了检查压力反射弧的中枢和传出部分，我们在记录动脉血压、心率和交感神经活动的同时，电刺激了乌拉坦麻醉的 Dahl 盐敏感大鼠和 Dahl 盐抵抗大鼠的主动脉减压神经。主动脉神经刺激在两组中产生了等效的反应，表明中枢和传出机制不能解释压力反射功能损害。在另一组 Dahl 大鼠中，当用去氧肾上腺素升高动脉血压时，记录多纤维传入主动脉压力感受器放电。高血压前期 Dahl 盐敏感大鼠的压力感受器激活明显少于 Dahl 盐抵抗大鼠，表明压力感受器放电受损是压力反射异常的原因。Dahl 品系之间的主动脉弓扩张性没有差异，这表明 Dahl 盐敏感大鼠的压力感受器放电受损可能不是由于血管壁扩张性异常。由于两种 Dahl 品系的动脉血压都在正常血压范围内，并且 Dahl 盐敏感大鼠和盐抵抗大鼠之间没有显著差异，压力感受器损害似乎是 Dahl 盐敏感大鼠的主要缺陷，而不是继发于高血压。我们推测，在动脉血压升高之前，Dahl 盐敏感大鼠的压力感受器功能损害可能导致 Dahl 盐敏感大鼠发生高血压的遗传倾向。
