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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© 2015 Published by Elsevier Inc.
