Objective: Catheter-based renal nerve ablation is a novel therapy for treatment-resistant hypertension. Although the precise mechanism is unknown, a reduction in global sympathetic tone and renal sympathetic tone, potentially resulting in a decrease in renin, may account for the antihypertensive effect.
Design and methods: In 17 patients (mean age 51.2 ± 9.4 years) with treatment-resistant hypertension (antihypertensive drugs 4.7 ± 1.3), office and ambulatory blood pressure (BP) measurements and circulating concentrations of catecholamines, renin, aldosterone and endothelin-1 were measured at baseline and 6 and 12 months after ablation. Office BP was measured for 1 h at 5-min intervals using an automatic device.
Results: Office BP (164.7 ± 27.7/102.3 ± 19.3 mmHg) decreased by 5.7 ± 18.8 mmHg (P = 0.11) systolic and by 2.6 ± 10.7 (P = 0.33) mmHg diastolic after 6 months, whereas after 12 months decreases were 12.7 ± 16.0 mmHg (P = 0.007) and 7.3 ± 11.9 mmHg (P = 0.02). Heart rate, 24-h (151.8 ± 12.6/94.2 ± 10.3 mmHg) and day and night ambulatory BP did not change, after either 6 or 12 months. Of the neurohormones, only plasma noradrenaline (397 pg/ml, interquartile range 268–461 pg/ml) decreased by 128 ± 167 pg/ml (P = 0.008) after 6 months, whereas other neurohormones remained unchanged. Forty-seven percent of patients had at least 10 mmHg decrease in 24-h ambulatory SBP. In these responders, office and ambulatory BP tended to be higher than in nonresponders, but neurohormones or changes after ablation between responders and nonresponders did not differ.
Conclusion: Renal nerve ablation in treatment-resistant hypertensive patients had a moderate effect on office BP and is associated with a decrease in plasma noradrenaline but not in renin. The absent decrease in renin may imply that the intensity of efferent renal denervation achieved with the number of ablations applied was insufficient.