title: Effect of acute blood pressure reduction on endothelial function in the brachial artery of patients with essential hypertension.
abstract: OBJECTIVE
  To evaluate the effect of acute blood pressure reduction on endothelium-dependent vasodilation in the peripheral circulation of essential hypertensive patients.
  
  
  METHODS
  A parallel group study; endothelial function measured in 64 essential hypertensive patients before and after (2 h) treatment with nifedipine (20 mg, n = 32) or captopril (50 mg, n = 32), p.o., randomly assigned.
  
  
  METHODS
  In hypertensive patients, we evaluated flow-mediated, endothelium-dependent dilation (FMD, high resolution ultrasound) of the brachial artery compared with endothelium-independent response to glyceryl trinitrate (GTN, 25 microg s.l.). Automatic computerized analysis was used to measure brachial artery diameter on end-diastolic frames acquired every second during the study. Sixty-six healthy normotensive subjects were also evaluated to assess the presence of endothelial dysfunction in hypertensive patients.
  
  
  RESULTS
  Hypertensive patients showed a significantly (P< 0.01) lower FMD (5.9 +/- 2.5%) as compared to healthy controls (7.7 +/- 3.8%). The response to GTN was similar in normotensive subjects (7.5 +/- 3.1%) and hypertensive patients (7.2 +/- 6.5%). At baseline brachial artery diameter, FMD and response to GTN were similar in the nifedipine- and captopril-treated groups. Nifedipine and captopril similarly reduced blood pressure, but only nifedipine increased heart rate. Acute nifedipine, but not captopril, significantly (P< 0.01) increased brachial artery diameter, while FMD and response to GTN were not modified after nifedipine or captopril.
  
  
  CONCLUSIONS
  Endothelial dysfunction in the brachial artery of essential hypertensive patients is not improved by acute blood pressure reduction.
authors.affiliation: Department of Internal Medicine, University of Pisa, Italy. l.ghiadoni@int.med.unipi.it
authors.forename: L
authors.initials: L
authors.lastname: Ghiadoni
authors.forename: Y
authors.initials: Y
authors.lastname: Huang
authors.forename: A
authors.initials: A
authors.lastname: Magagna
authors.forename: S
authors.initials: S
authors.lastname: Buralli
authors.forename: S
authors.initials: S
authors.lastname: Taddei
authors.forename: A
authors.initials: A
authors.lastname: Salvetti
mesh_terms: D000328:Adult; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use*; D000959:Antihypertensive Agents / Q000627:therapeutic use*; D001794:Blood Pressure / Q000187:drug effects*; D001916:Brachial Artery / Q000000981:diagnostic imaging / Q000503:physiopathology*; D002121:Calcium Channel Blockers / Q000627:therapeutic use*; D002216:Captopril / Q000627:therapeutic use*; D003326:Coronary Circulation; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D006801:Humans; D006973:Hypertension / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D009543:Nifedipine / Q000627:therapeutic use*; D005996:Nitroglycerin / Q000627:therapeutic use; D012016:Reference Values; D014463:Ultrasonography; D014664:Vasodilation; D014665:Vasodilator Agents / Q000627:therapeutic use
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D000959:Antihypertensive Agents; D002121:Calcium Channel Blockers; D014665:Vasodilator Agents; D002216:Captopril; D005996:Nitroglycerin; D009543:Nifedipine