Renal denervation (RD) does not prevent the hypertensive response to chronic baroreceptor unloading (CBU) in the dog

Abstract

We have reported that CBU causes a sustained increase in mean arterial pressure (MAP) in the dog (AJP 288: R863-R871, 2005). In the present study, we tested the hypothesis that the renal nerves are essential for the increase in MAP following CBU. Dogs (n=5) were housed in metabolism cages to determine daily sodium excretion and MAP was recorded continuously via telemetry (DSI International). After four control days, the carotid artery proximal to an innervated carotid sinus was ligated to produce CBU (all other baroreceptive areas previously denervated). After seven days of CBU, the ligature was removed. Subsequently, the kidneys were denervated bilaterally and at least 14 days later, the experimental protocol was repeated. The average MAP (in mmHg ± 1SE) in the Control, CBU and Recovery periods are shown in the table below. ANOVA indicated a significant effect of CBU on MAP but no effect of RD on the MAP response to CBU and no interaction between the CBU and RD factors. There was a significant increase in renal sodium excretion on the first day of CBU in both treatment conditions but sodium excretion returned to control levels thereafter. We conclude that the renal nerves are not required to sustain the increase in MAP caused by seven days of CBU in the dog. (Supported by HL 67329)