title: Normal erythrocyte calpain I activity on membrane proteins under near-physiological conditions in patients with essential hypertension.
abstract: BACKGROUND
  It has been reported that the equilibrium between the erythrocyte protease calpain I and its physiological inhibitor calpastatin is disrupted in patients with essential hypertension.
  
  
  OBJECTIVE
  To investigate the activity of non-purified calpain I in hemolysates against the erythrocytic membrane proteins, rather than against other substrates.
  
  
  METHODS
  Evaluation of calpain I red cell activity upon its own physiological substrates in hypertensive patients, in a near-physiological environment.
  
  
  METHODS
  LIM-23 and LIM-40 of Hospital das Clinicas of the Faculty of Medicine of USP.
  
  
  METHODS
  Patients with moderate primary hypertension over 21 years of age who were given amlodipine (n:10) and captopril (n:10) for 8 weeks, plus normal controls (n:10).
  
  
  METHODS
  Red cell membrane proteins were incubated with and without protease inhibitors and with and without calcium chloride and underwent polyacrylamide gel electrophoresis.
  
  
  RESULTS
  Digestion of bands 2.1 and 4.1 was observed, indicating calpain I activity. No statistical differences regarding bands 2.1 and 4.1 were observed before treatment, between the controls and the hypertensive patients, either in ghosts prepared without calcium or with increasing concentrations of calcium. Nor were statistical differences observed after treatment, between the controls and the patients treated with amlodipine and captopril, or between the patients before and after treatment with both drugs.
  
  
  CONCLUSIONS
  The final activity of non-purified calpain I upon its own physiological substrate, which was the approach utilized in this study, may more adequately reflect what happens in red cells. Under such conditions no imbalance favoring calpain I activity increase was observed. The protective factor provided by calpastatin against calpain I activity may diminish under hypertension.
authors.affiliation: LIM-234 and LIM-40, Hospital das Clinicas, Faculty of medicine, Universidade de São Paulo, São Paulo, Brazil.
authors.forename: Tereza Maria
authors.initials: TM
authors.lastname: Dantas de Medeiros
authors.forename: Katia Coelho
authors.initials: KC
authors.lastname: Ortega
authors.forename: Décio
authors.initials: D
authors.lastname: Mion
authors.forename: Kimiyo
authors.initials: K
authors.lastname: Nonoyama
authors.forename: Orlando Cesar de Oliveira
authors.initials: OC
authors.lastname: Barretto
mesh_terms: D000328:Adult; D017311:Amlodipine / Q000627:therapeutic use; D017487:Ankyrins / Q000378:metabolism; D002135:Calcium-Binding Proteins / Q000378:metabolism; D002154:Calpain / Q000097:blood / Q000502:physiology*; D002216:Captopril / Q000627:therapeutic use; D016022:Case-Control Studies; D004591:Electrophoresis, Polyacrylamide Gel; D004910:Erythrocyte Membrane / Q000201:enzymology*; D006801:Humans; D006973:Hypertension / Q000188:drug therapy / Q000201:enzymology*; D008565:Membrane Proteins / Q000097:blood / Q000502:physiology*
chemical_list: C110202:ANK1 protein, human; D017487:Ankyrins; D002135:Calcium-Binding Proteins; D008565:Membrane Proteins; D017311:Amlodipine; C033668:calpastatin; D002216:Captopril; D002154:Calpain