title: Renal resistance and long-term blood pressure in individuals genetically predisposed for essential hypertension: 10-year follow-up of the Danish Hypertension Prevention Project.
abstract: Young individuals genetically predisposed for essential hypertension have increased renal vascular resistance. We evaluated whether 1 year of angiotensin II receptor blockade decreases afferent arteriolar resistance (RA) and induces a sustained blood pressure (BP) reduction during a 10-year follow-up period in offspring of parents both diagnosed with essential hypertension.
  
  
  
  Based on renal plasma flow (p-aminohippurate clearance) and glomerular filtration rate (Cr-EDTA clearance) RA was calculated according to the model originally established by Gomez. Following baseline measurements, the participants (n = 110, mean age 30 years) were randomly allocated to 12 months of treatment with either candesartan or placebo followed by repetition of measurements and withdrawal of medication. Four-hour ambulatory BP (ABP) was recorded at baseline, by end of active treatment and after 6 months, 1, 2, 3, 5, and 10 years. ABP was analyzed according to RA achieved at the end of active treatment.
  
  
  
  Candesartan reduced RA by 14% (P < 0.01). Ten years posttreatment systolic ABP increased by 2.1 mmHg (P = 0.04) and diastolic by 4.2 mmHg (P < 0.01) compared with baseline, without any difference between treatment arms. A high posttreatment RA was associated with higher BP levels during follow-up, but long-term alterations in 24-h BP were similar in participants with low and high RA and not different between treatment arms.
  
  
  
  RA is associated with 24-h BP levels, but temporary lowering of BP and RA by candesartan does not prevent BP from increasing further. Prevention of hypertension appears not feasible by short-term inhibition of the rennin-angiotensin system in young adults.
authors.affiliation: aInstitute of Clinical Medicine, Aarhus University, Aarhus bDepartment of Nephrology, Aalborg University Hospital, Aalborg cInstitute of Biomedicine, Aarhus University dDepartment of Cardiology eDepartment of Renal Medicine, Aarhus University Hospital, Aarhus, Denmark.
authors.forename: Niels H
authors.initials: NH
authors.lastname: Buus
authors.forename: Michael J
authors.initials: MJ
authors.lastname: Mulvany
authors.forename: Hans
authors.initials: H
authors.lastname: Eiskjær
authors.forename: Kent L
authors.initials: KL
authors.lastname: Christensen
authors.forename: Karin
authors.initials: K
authors.lastname: Skov
mesh_terms: D000328:Adult; D057911:Angiotensin Receptor Antagonists / Q000627:therapeutic use; D000959:Antihypertensive Agents / Q000627:therapeutic use*; D001160:Arterioles / Q000503:physiopathology; D001562:Benzimidazoles / Q000627:therapeutic use*; D001713:Biphenyl Compounds; D001794:Blood Pressure / Q000187:drug effects*; D018660:Blood Pressure Monitoring, Ambulatory; D003718:Denmark; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D006973:Hypertension / Q000235:genetics / Q000503:physiopathology / Q000517:prevention & control*; D008297:Male; D012084:Renin-Angiotensin System / Q000187:drug effects; D013777:Tetrazoles / Q000627:therapeutic use*; D013997:Time Factors; D014655:Vascular Resistance / Q000187:drug effects*
chemical_list: D057911:Angiotensin Receptor Antagonists; D000959:Antihypertensive Agents; D001562:Benzimidazoles; D001713:Biphenyl Compounds; D013777:Tetrazoles; C081643:candesartan