Cardiac hypertrophy depends upon sleep blood pressure: a... : Journal of Hypertension (original) (raw)

Original article

a study in rats

Morgan, Trefor O.1,3; Brunner, Hans R.2; Aubert, Jean-Francois2; Wang, Qing2; Griffiths, Cory1; Delbridge, Lea1

1Department of Physiology, University of Melbourne, Australia

2Hypertension Unit, University of Vaud, Lausanne, Switzerland.

3Correspondence and requests for reprints to Professor T.O. Morgan, Department of Physiology, University of Melbourne, Parkville, Victoria 3052, Australia.

Sponsorship: Supported by the National Heart Foundation of Australia and the Roche Foundation, Switzerland.

Tel: +61 3 9344 5846; fax: +61 3 9344 0189; email: [email protected]

Received 29 July 1999 Revised 7 December 1999 Accepted 4 January 2000

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 intraperitoneally 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.

Conclusion

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.