title: Blood pressure and neurohormonal responses to renal nerve ablation in treatment-resistant hypertension.
abstract: 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.
  
  
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: aDivision of Pharmacology and Vascular Medicine, Department of Internal Medicine bDepartment of Radiology, Erasmus MC, Rotterdam, the Netherlands.
authors.forename: Mustafa
authors.initials: M
authors.lastname: Ezzahti
authors.forename: Adriaan
authors.initials: A
authors.lastname: Moelker
authors.forename: Edith C H
authors.initials: EC
authors.lastname: Friesema
authors.forename: Nicole A J
authors.initials: NA
authors.lastname: van der Linde
authors.forename: Gabriel P
authors.initials: GP
authors.lastname: Krestin
authors.forename: Anton H
authors.initials: AH
authors.lastname: van den Meiracker
mesh_terms: D000328:Adult; D000450:Aldosterone / Q000097:blood*; D000959:Antihypertensive Agents / Q000627:therapeutic use*; D001794:Blood Pressure; D001795:Blood Pressure Determination; D003714:Denervation / Q000379:methods*; D004351:Drug Resistance; D019332:Endothelin-1 / Q000097:blood*; D006801:Humans; D006973:Hypertension / Q000188:drug therapy / Q000503:physiopathology / Q000628:therapy*; D007668:Kidney / Q000294:innervation*; D008875:Middle Aged; D012083:Renin / Q000097:blood*
chemical_list: D000959:Antihypertensive Agents; D019332:Endothelin-1; D000450:Aldosterone; D012083:Renin