Cardiac hypertrophy depends upon sleep blood pressure: a study in rats

Objective The objective of this study was to determine whether cardiac hype rtrophy in hypertensive rats could be reduced and normalized by intermitten t reduction of blood pressure, and to determine whether left ventricular hy pertrophy 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 th e left renal artery. Blood pressure response was monitored using a telemetr y system (Data Science International). Blood pressure was reduced for varyi ng periods of the day by giving different doses of captopril in the drinkin g water or by intra-peritoneal administration, Cardiac size was measured by weighing the ventricles and factoring by the body weight to obtain a cardi ac index. Results Captopril 75 mg/kg per day and 25 mg/kg per day in the drinking wat er administered between 1800 and 2000 h lowered the 24 h blood pressure mor e than captopril 15 mg/kg per day or 5 mg/kg per day intra-peritoneally giv en at 0800 h. Captopril 75 mg/kg per day and captopril 15 mg/kg per day (in tra-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 pre ssure). Twenty-four hour cardiac work did not correlate with the response. Conclusion Cardiac hypertrophy can be reduced by intermittent treatment of elevated blood pressure. It is also caused by intermittent elevation of blo od pressure. It appears that the crucial factor is when these alterations i n 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 wai l stress is the signal to initiate the events that lead to cardiac hypertro phy but this only occurs if the hormonal milieu is appropriate. J Hypertens 2000, 18:445-451 (C) Lippincott Williams & Wilkins.