Role of afferent and efferent renal nerves in mediating cardiovascular responses to renal denervation in experimental hypertension

      Studies in animal models suggest a role for renal nerves in the pathogenesis and maintenance of hypertension (HTN). Much of this evidence is based on the effect of renal denervation (RDNX) on arterial pressure (AP). However, the magnitude of the AP response to RDNX is not uniform across experimental models suggesting renal nerves contribute to some forms of hypertension more than others. Using a recently developed model for targeted ablation of renal afferent nerves, we compared the effect of total renal denervation (tRDNX; afferent + efferent) to selective afferent RDNX (aRDNX) in development of AngII-salt and DOCA-salt hypertension. Neither tRDNX nor aRDNX affected development of AngII-salt HTN. In contrast, tRDNX and aRDNX both attenuated DOCA-salt HTN by 50%. We also tested the ability of tRDNX and aRDNX to reverse established HTN in Dahl salt sensitive (DS) rats. tRNDX decreased AP in DS rats ~10 mmHg after 3 or 9 weeks of high salt diet. In contrast, aRDNX had no effect on AP in DS rats at any time point. We conclude that 1) tRDNX has no effect on the pathogenesis of AngII-salt HTN, 2) attenuation of DOCA-salt HTN by tRDNX is due entirely to ablation of renal afferent nerves and 3) AP responses to tRDNX in the established phase of DS HTN is entirely mediated by ablation of renal efferent nerves. Supported by NIH HL116476.
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