Sympathetic Innervation Modulates the Expression of Angiotensin II Receptors in Embryonic Rat Heart Graftedin Oculo

Angiotensin II acts as a cardiac growth factor, and causes both inotropic and chronotropic changes within the heart. In the present study, we used anin oculomodel system to examine the effects of sympathetic innervation on the density of cardiac angiotensin II receptors. Quantitative autoradiography was used to determine the density of angiotensin II receptors in embryonic rat hearts grafted into either sympathetically innervated or sympathetically denervated eye chambers of adult host rats. The density of specific binding to angiotensin II receptors was nearly three-fold higher in sympathetically non-innervated compared to sympathetically innervated heart grafts (30.8±4.2v11.5±3.2 fmol/mg protein). Specific binding to angiotensin II receptors in heart grafts was displaced by addition of the AT1receptor antagonist losartan, but not by addition of the AT2receptor competitor PD 123177. Thus, only AT1receptors were present in sympathetically innervated and sympathetically non-innervated embryonic rat hearts graftedin oculo. We conclude that changes in sympathetic innervation caused changes in the density of cardiac angiotensin II receptors in the present study. Our results may have implications for growth and function not only during cardiac development, but also during cardiac disease.