Drinking-induced bradyarrhythmias and cerebral injury in Dahl salt-sensitive rats with sinoaortic denervation

Abstract

We have demonstrated that a drinking-induced pressor response was larger if the baroreflex did not operate, and the mean arterial pressure reached 163 mmHg in conscious rats with sinoaortic denervation (SAD). Thus we hypothesized that a drinking behavior became a cardiovascular risk factor if a basal arterial pressure was high. To clarify this, we analyzed the occurrence of arrhythmias and the accumulation of microglia in Dahl salt-sensitive rats (Dahl S) with SAD. We maintained Dahl S and Dahl salt-resistant rats (Dahl R) with a high-sodium diet for 5 weeks. After SAD surgery, we measured arterial pressure and electrocardiogram during water-drinking behavior in all rats. Furthermore, we measured tumor necrosis factor-α concentration in the cerebrospinal fluid (CSF) and microglial accumulations around the third and fourth ventricles in rats with programmed drinking at a rapid or slow rate for 7 days. Incidences of drinking-induced bradyarrhythmias and premature ventricular contractions (PVCs) were significantly larger in Dahl S than Dahl R rats. Both bradyarrhythmias and PVCs were completely abolished by atropine administration. Accumulations of microglia around the third ventricle and increases in TNF-α in the CSF were observed in rats that drank water at a rapid rate; these were not seen in rats that drank water slowly. In conclusion, both cardiovascular events and cerebral injury may be increased by drinking in Dahl S rats with SAD. These risks are reduced by modifying drinking behavior such as slowing the drinking rate.