Role of Adenosine 3′,5′-Monophosphate in Maturation of Fetal Lungs

Abstract

Extract: Fetal lung cyclic AMP phosphodiesterase, cyclic AMP, phosphatidyl choline, and incorporation of precursors into phosphatidyl choline were measured in rabbits after maternal administration of hydrocortisone phosphate and aminophylline. Both agents inhibited lung phosphodiesterase activity and augmented cyclic AMP concentrations (Table 1). Aminophylline administration was associated with a significant increase in lung saturated phosphatidyl choline (Table 2). Incorporation of [¹⁴C]choline and [³H]methionine was increased by both aminophylline and hydrocortisone (Table 3).

Speculation: Aminophylline, which inhibits cyclic AMP phophodiesterase as its primary mode of action, has effects similar to hydrocortisone on incorporation of labeled precursors into phosphatidyl choline. Cyclic AMP, therefore, may be a mediator of maturation of lung phosphatidyl choline synthesis and/or secretion in the fetus, and pharmacologic agents which enhance cyclic AMP levels in the lungs may also enhance synthesis of phosphatidyl choline.

Log in or create a free account to read this content

Gain free access to this article, as well as selected content from this journal and more on nature.com

Access through your institution

or

Sign in or create an account

Continue with Google

Continue with ORCiD