Impact of renal denervation on tissue Na content in treatment-resistant hypertension.

OBJECTIVES

Renal denervation (RDN) has been introduced for reducing blood pressure (BP) in treatment-resistant hypertension (TRH). The precise mechanism how RDN exerts its BP-lowering effects are not yet fully understood. It is widely accepted that sodium (Na) plays a crucial role in the pathogenesis of hypertensive disease. However, there is increasing evidence of osmotically inactive Na storage. We investigated the impact of RDN on Na homeostasis using estimation of salt intake, and measurement of tissue Na content.

METHODS

In a study 41 patients with TRH (office BP ≥140/90 mmHg and diagnosis confirmed by 24-h ambulatory BP monitoring) underwent RDN. Tissue Na content was assessed non-invasively with 3.0 T magnetic resonance imaging before and 6 months after RDN. In addition, 24-h urinary Na excretion as an estimate of salt intake and spot urine Na/K excretion were assessed. The study was registered at http://www.clinicaltrials.gov (ID: NCT01687725).

RESULTS

There was a significant fall in BP (office: -17 ± 20/-10 ± 12 mmHg; 24-h: -11 ± 13/-6 ± 9 mmHg, all p < 0.001) 6 months after RDN. In contrast, tissue Na content of the muscle (20.1 ± 3.9 vs. 20.7 ± 4.0 mmol/L, p = 0.229) and skin (24.4 ± 6.5 vs. 24.8 ± 6.6 mmol/L, p = 0.695) did not change after RDN. Moreover, there was also no change in salt intake after RDN, whereas Na/K ratio only acutely increased.

CONCLUSIONS

Although RDN resulted in a substantial reduction of BP, tissue Na content of the muscle and skin was not mobilized and reduced. These data indicate that the BP reduction after RDN is unrelated to Na homeostasis.