Ontogeny of food deprivation effects on ornithine decarboxylase: ornithine decarboxylase induction by alpha and beta agonists.

Short-term food deprivation (FD) of preweanling rat pups causes a marked and specific suppression of liver ornithine decarboxylase (ODC) induction by alpha and beta adrenergic agonists that is mediated by postreceptor mechanisms. In the present study, we demonstrate that FD also affects the ability of adrenergic agonists to induce hepatic ODC in older animals and that these changes differ from those occurring in neonates in the duration of FD associated with changes, the subcellular mechanisms involved and the organ specificity of the effect. FD (48 hr) of 30-day-old rats caused a specific suppression of liver ODC induction by the alpha agonist phenylephrine whereas the effect of the beta agonist isoproterenol was not changed. ODC induction by vasopressin or angiotensin was unaffected, whereas the effect of aminophylline was potentiated. FD of 30-day-old rats caused a marked suppression of both alpha and beta agonist action in the heart. FD of mature (60-day-old) rats was associated with an enhanced hepatic ODC response to phenylephrine and isoproterenol. Whereas the number of receptors in heart assessed by the binding of [3H]prazosin and [125I]pindolol to alpha and beta receptors, respectively, decreased in parallel with changes in responsivity, liver ODC responses did not correlate well with receptor changes. These findings support previous findings of altered sympathetic responsivity in heart, liver and fat during FD and indicate that the sympathetic nervous system responds to FD with a complex series of changes in both pre- and postsynaptic mechanisms.