Stimulation of the β-ARs via isoproterenol causes a down regulation of receptor
activity via loss of high-affinity binding in the receptor and not receptor number (Marsh
et al. 1985). So alternatively, β-AR blockade could have conversely prompted
cardiomyocytes to up-regulate receptor function via either adenylate cyclase stimulation
of coupling, increasing binding affinity, or increasing protein synthesis and over-
sensitize the cell to catecholamines. If over-stimulation by baseline catecholamines was
taking place, this may have simulated the occurrence of early sympathetic innervation.
β-AR stimulation in rats inhibited further cell division and DNA synthesis in the atria
thereby causing the transition in heart development from hyperplasia to hypertrophy-
mediated growth (Tucker & Gist, 1986). If a similar effect occurred in the chronically
atenolol-treated embryos, it could mean that Mesonephros group hearts were larger due
to pathological hypertrophy. This excess growth in cardiomyocytes can cause less
efficient pumping as seen in older human patients suffering from heart failure. Inefficient
pumping causes insufficient filling and thus decreased cardiac output but can also cause back up of fluids due to insufficient pumping and consequently edema (Mohrman
et al. 2010).