Abstract

Renal hypertension has been shown to be prevented and reversed by renal denervation. It has been postulated that the afferent nerves from the kidney are responsible for mediating the hypertensive stimulus that activates the sympathetic nervous system and increases arterial pressure. This study was designed to directly test the hypothesis that the afferent renal nerves are necessary for the development and maintenance of renal hypertension. In the first experiment, dorsal spinal rhizotomies or sham rhizotomies were performed in rats between T9 and L1, through which afferent renal nerves have been shown to traverse. After the one-kidney, one-wrap procedure, the increase in systolic arterial pressure and water intake was similar in the two groups of rats. To determine whether the removal of afferent renal nerves reversed the hypertensive process, animals with established renal hypertension were subjected to dorsal rhizotomy or the sham-rhizotomy procedure. Again, there was no significant effect on systolic arterial pressure and water intake. Although combined dorsal and ventral rhizotomy and subdiaphragmatic vagotomy did not affect the onset of hypertension, spinal transection at the level of C8 effectively prevented the rise in arterial pressure. Although efferent neural mechanisms contribute to the hypertensive process, these studies suggest that afferent renal nerves are not directly involved in the development and maintenance of one-kidney, one-wrap renal hypertension.

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