Dietary sodium loading elevates blood pressure in baroreceptor denervated rats

We have examined the possibility that defective baroreflex function may contribute to the hypertensive effect of a high dietary sodium intake. In a preliminary study we found that, after interrupting the baroreflex by sino-aortic denervation (SAD), feeding a high-sodium diet to normotensive Wistar/Kyoto rats (WKY) caused their tail-cuff blood pressure to rise to hypertensive levels. In the present study, SAD and sham-operated WKY were fed diets with either a low or a high sodium content. An increase in the sensitivity of blood pressure to sodium after baroreceptor denervation was confirmed by direct measurement of mean arterial pressure (MAP) in conscious rats via indwelling aortic catheters. After 8 weeks the MAP in SAD rats on the high sodium diet was 35 mm Hg higher than in SAD rats on the low sodium diet. Ganglion blockade reduced MAP to a similar level in all treatment groups, but pressor responses to phenylephrine were greater in SAD rats on the high sodium diet, suggesting that the hypertensive effect of sodium in this group might have been due to increased sympathetic vasoconstriction.