Russ R, Abdel-Rahman A R, Wooles W R
Department of Pharmacology, School of Medicine, East Carolina University, Greenville, NC 27858.
Alcohol. 1991 Jul-Aug;8(4):301-7. doi: 10.1016/0741-8329(91)90433-w.
The present study investigated the role of the sympathetic nervous system in the development of ethanol-induced hypertension (EIH) in the rat. Sympathetic nerve activity (SNA) as an index of central sympathetic tone was measured directly from the preganglionic fibers of the greater splanchnic nerve. Four weeks after starting ethanol feeding, and prior to the development of hypertension, SNA of the ethanol-fed rats was significantly greater than that of controls. The increase in SNA was also evident at the early stages of EIH, at 8 weeks, and in fully developed EIH, after 12 weeks of ethanol consumption. Baroreceptor reflex control of heart rate (HR) but not SNA was impaired prior to the development of EIH at 4 weeks. However, at 8 and 12 weeks, baroreflex control of HR and SNA was normal or slightly greater than that of control rats. Because arterial pressure of ethanol-fed rats was significantly higher than that of controls at 8 and 12 weeks, the data suggest that ethanol feeding caused baroreceptor resetting. Pressor responsiveness to phenylephrine was depressed before the development of EIH but was similar to that of control rats following the development of EIH. The data also shows that blood and plasma volumes of ethanol-fed rats at the times that coincided with the pre- and posthypertensive states were similar to those of control rats which suggests that the development of EIH does not involve an increase in plasma volume. It is concluded that an increase in SNA contributes to the development of EIH and that baroreceptor resetting evoked by ethanol feeding plays a permissive role in maintaining an elevated blood pressure in ethanol-fed rats.
本研究调查了交感神经系统在大鼠乙醇诱导性高血压（EIH）发展过程中的作用。作为中枢交感神经张力指标的交感神经活动（SNA）是直接从大内脏神经的节前纤维测量的。开始给予乙醇四周后，在高血压发展之前，给予乙醇的大鼠的SNA显著高于对照组。在EIH的早期阶段（8周时）以及在摄入乙醇12周后完全发展的EIH阶段，SNA的增加也很明显。在4周EIH发展之前，心率（HR）的压力感受器反射控制受到损害，但SNA不受影响。然而，在8周和12周时，HR和SNA的压力反射控制正常或略高于对照大鼠。由于在8周和12周时，给予乙醇的大鼠的动脉压显著高于对照组，数据表明给予乙醇导致了压力感受器重置。在EIH发展之前，对去氧肾上腺素的升压反应性降低，但在EIH发展之后与对照大鼠相似。数据还表明，在与高血压前期和后期状态一致的时间点，给予乙醇的大鼠的血液和血浆量与对照大鼠相似，这表明EIH的发展不涉及血浆量的增加。结论是，SNA的增加促成了EIH的发展，并且给予乙醇引起的压力感受器重置在维持给予乙醇的大鼠的高血压状态中起允许作用。
