title: Cardiac hypertrophy depends upon sleep blood pressure: a study in rats.
abstract: OBJECTIVE
  The objective of this study was to determine whether cardiac hypertrophy in hypertensive rats could be reduced and normalized by intermittent reduction of blood pressure, and to determine whether left ventricular hypertrophy was related to 24 h workload or peak blood pressure responses.
  
  
  METHODS
  Hypertension was created by the application of a 0.20 mm clip to the left renal artery. Blood pressure response was monitored using a telemetry system (Data Science International). Blood pressure was reduced for varying periods of the day by giving different doses of captopril in the drinking water or by intra-peritoneal administration. Cardiac size was measured by weighing the ventricles and factoring by the body weight to obtain a cardiac index.
  
  
  RESULTS
  Captopril 75 mg/kg per day and 25 mg/kg per day in the drinking water administered between 1800 and 2000 h lowered the 24 h blood pressure more than captopril 15 mg/kg per day or 5 mg/kg per day intra-peritoneally given at 0800 h. Captopril 75 mg/kg per day and captopril 15 mg/kg per day (intra-peritoneal) caused regression of cardiac hypertrophy whereas the other doses had no effect The best predictor of the cardiac hypertrophy response was the blood pressure between 0800 and 1200 h (i.e. the sleeping blood pressure). Twenty-four hour cardiac work did not correlate with the response.
  
  
  CONCLUSIONS
  Cardiac hypertrophy can be reduced by intermittent treatment of elevated blood pressure. It is also caused by intermittent elevation of blood pressure. It appears that the crucial factor is when these alterations in blood pressure take place. An elevated blood pressure during the sleeping hours causes left ventricular hypertrophy, whereas a normal blood pressure during the sleeping hours allows reduction. It is suggested that acute wall stress is the signal to initiate the events that lead to cardiac hypertrophy but this only occurs if the hormonal milieu is appropriate.
authors.affiliation: Department of Physiology, University of Melbourne, Parkville, Victoria, Australia. t.morgan@physiology.unimelb.edu.au
authors.forename: T O
authors.initials: TO
authors.lastname: Morgan
authors.forename: H R
authors.initials: HR
authors.lastname: Brunner
authors.forename: J F
authors.initials: JF
authors.lastname: Aubert
authors.forename: Q
authors.initials: Q
authors.lastname: Wang
authors.forename: C
authors.initials: C
authors.lastname: Griffiths
authors.forename: L
authors.initials: L
authors.lastname: Delbridge
mesh_terms: D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology; D001794:Blood Pressure / Q000187:drug effects; D002216:Captopril / Q000494:pharmacology; D002302:Cardiac Output; D006332:Cardiomegaly / Q000209:etiology*; D004305:Dose-Response Relationship, Drug; D006973:Hypertension / Q000150:complications* / Q000473:pathology / Q000503:physiopathology*; D009206:Myocardium / Q000473:pathology; D009929:Organ Size; D051381:Rats; D017208:Rats, Wistar; D012890:Sleep; D013686:Telemetry
chemical_list: D000959:Antihypertensive Agents; D002216:Captopril