α-Adrenergic Receptor Agonists Stimulate Ribosome Formation in Hearts from Enalapril-Treated Piglets

Hearts from untreated or enalapril-treated piglets were used to measure rates of ribosome formation and total protein synthesis during perfusion as modified Langendorff preparations. Pretreatment of newborn piglets with enalapril maleate (5 mg, once daily for 3 days) resulted in a decreased rate of growth of the left ventricle. Addition of 1 μM angiotensin II to the perfusate had no effect on in vitro ribosome formation or protein synthesis in either the right or left ventricle of hearts from untreated or enalapril-treated piglets. Angiotensin II receptor number or affinity in the left ventricle was not decreased by enalapril treatment. In contrast, addition of combination of 1 μM norepinephrine and 1 μM propranolol or 1 μM phenylephrine and 1 μM propranolol to the perfusate restored the rate of ribosome formation in the left ventricle of hearts from enalapril-treated piglets to that observed in the left ventricle of hearts from untreated piglets. Prazosin (100 nM) blocked the stimulatory effect of either norepinephrine or phenylephrine on ribosome formation in the left ventricle. Binding of [3H] prazosin to membranes from the left ventricle was unaltered by pretreatment of the piglet with enalapril maleate. Pretreatment of piglets with prazosin (1 mg, twice daily for 3 days) resulted in a small but significant decrease in mean arterial pressure as well as the rate of left ventricular growth. Pretreatment of piglets with hydralazine (10 mg, twice daily for 3 days) significantly reduced mean arterial pressure but did not alter left ventricular growth. These results support a role for α1-adrenergic receptor stimulation in the regulation of neonatal cardiac growth.