Role of the sympathetic nervous system in ethanol-induced hypertension in rats.

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.