Increased Dietary Salt Enhances Sympathoexcitatory and Sympathoinhibitory Responses From the Rostral Ventrolateral Medulla

Adams JM, Madden CJ, Sved AF, Stocker SD.

Department of Physiology, University of Kentucky, 800 Rose St MS-508, Lexington, KY 40536-0298, USA

Hypertension. 2007 Aug;50(2):354-9. Epub 2007 Jun 25.

It is widely believed that increase in dietary salt intake can elevate arterial blood pressure (ABP) through neurogenic mechanisms. In this study the authors investigated whether this increase in pressure response due to dietary salt intake involves elevated sympathetic nerve activity and whether these responses could be balanced by inhibitory inputs to RVLM neurons. In order to test this the authors used male SD rats. The animals were divided into groups and given either water or 1% NaCl solution for 14 days. All the animals were fed with normal chow diet. When glutamate (excitatory neurotransmitter)  was microinjected into the RVLM at four different doses there was increase in the renal and splanchnic nerve activity and ABP in the rats that were given salt in water compared to normal water. Another set of animals were microinjected with GABA (gamma amino butyric acid, inhibitory neurotransmitter) at three different doses and there was a decrease in both the renal and splanchnic nerve activity and ABP in rats consuming water with salt compared to control animals with normal water. In this study the authors were also interested to know the time course of the sympathoexcitatory and sympathoinhibitory responses. In order to do that rats were divided into groups and given 1% salt and water. The rats were microinjected with glutamate and GABA in the RVLM on days 1,7, 14 and 21. Renal SNA and ABP were significantly different in 1% NaCl drinking group compared to the control when microinjected on 14 and 21 days but not after 1 and 7 days. In the first experiment both the renal and splanchnic nerve activity were measured however in the second experiment only renal activity alone was measured. The fact that both the nerve activity were significantly elevated in the first study raises the question why renal nerve activity alone is measured in the second study? Finally the authors investigated whether the enhanced responsiveness to 1% NaCl in water persisted even after the rats were returned to a normal salt diet. After 14 days of 1% NaCl in the drinking water the rats were given normal water. The changes in renal SNA and ABP persisted for 1 day but not for 7 days. The authors conclude that mechanism by which elevated dietary salt increases the pressor response is through increased SNA response.