Abstract

Introduction

Materials & Methods

Results

Discussion & Conclusion

References

Discussion
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This study examined the response of both cell growth and apoptosis in the heart and aorta of spontaneoulsy hypertensive rats during beta-adrenergic blockadde therapy. Rats were treated or not with propranolol (50 mg/kg/day) for 2 or 4 weeks starting at 10-11 week of age. DNA synthesis was measured by [3H]-thymidine incorporation in vivo. Apoptosis was quantified by radiolabeling of 3'-OH ends in the extracted DNA with terminal deoxynucleotidyl transferase, followed by gel electrophoresis and quantification by PhosphoImager of radioactivity in oligonucleeosomal DNA fragments.After 4 weeks of treatment, although propranolol did not decrease systolic blood pressure significantly, the heart rate was lowered by 20% (vs control: 360+17 beats per minute). In the aorta, propranolol failed to affect vascular growth and apoptosis. In contrast, in the heart we observed that a 4-week treatment caused a significant 3- to 4-fold in apoptosis (vs control: 0.4+0.1 arbitrary units/ ug DNA; P < 0.05) and a regression of hypertrophy as measured by the heart to body weight ratio (by 11% vs control: 5.2+0.1 x 10E-3). These effects were preceded by a transient reduction in DNA synthesis (by 17% vs control: 831+31 cpm/100ug DNA; P < 0.05) at 2 weeks of therapy. Taken together, these results suggest that beta-blockade stimulate apoptosis (1) in an organ-specific manner, i.e. in the heart but not the aorta at 4 weeks of therapy, and (2) independently of blood pressure reduction. Supported by MRCC and FRSQ.

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Presentation Number SAdeblois0801
Keywords: apoptosis, beta-blockers, SHR, growth, smooth muscle