Regulation of beta-adrenergic receptor density in the non-innervated and denervated embryonic chick heart.

Factors which regulate beta-adrenergic receptor density in non-innervated and denervated embryonic tissues have not been fully elucidated. In the present study, the effects of exposure to isoproterenol and propranolol on beta-adrenergic receptor density in the non-innervated (preneural) and partially innervated (neural) embryonic chick heart are examined. In addition, the effects of chemical and surgical sympathectomy on cardiac beta-adrenergic receptor density in the chick embryo are investigated. (125I)-pindolol was used as a receptor probe. The density of beta-adrenergic receptors in the embryonic chick heart peaks on incubation day 9 (664 fmols/mg protein) and then decreases by more than 80% by incubation day 19. Administration of propranolol or isoproterenol on incubation days 4 to 6 results in no change or a decrease (to 62% of control), respectively, in receptor density on incubation day 7. Administration of propranolol on incubation days 10 to 19 causes an increase (to 230% of control) in beta-adrenergic receptor density on day 20. Administration of isoproterenol on incubation days 10 to 16 results in a decrease (to 26% of control) in receptor density on day 17. Neither chemical sympathectomy, produced by administration of 6-hydroxydopamine, nor surgical sympathectomy, produced by removal of premigratory neural crest cells, significantly alters cardiac beta-adrenergic receptor density from control values. Administration of adrenergic drugs produces a greater change in beta-adrenergic receptor density after sympathetic innervation (day 10) than in preneural hearts. This indicates that sympathetic nerves influence the properties of beta-adrenergic receptors during embryonic development.