Beta-adrenergic receptors elevate cAMP. This results in increased contractility in the heart while it results in reduced contractility in vascular tissue. Thus, we think that the organ selectivity for apoptosis induction with beta blockers may reflect the differential response to cAMP in these two tissues. Incidentally, it is intersting to note that long term blood pressure reduction with beta blockers in hypertensive patients does not result in a normalization of the wall to lumen ratio in peripheral arteries. (in constrast to ACE inhibitors for instance).
In our experiments in SHR, propranolol for 4 weeks did not reduce systolic pressure although heart rate was disminished. The SHR is not a very responsive model if you try to reverse established hypertension over a few weeks.
We don't know if WKY would respond to beta blockers. We have tested nifedipine in WKY and sawq no effect on either vascular or cardiac apoptosis, DNA synthesis, DNA content or on systolic blood pressure (abstract in Hypertension, sept 97).
The SHR appears to be particularly prone to apoptosis induction as compared to normotensive rat strains.