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Extract: Renal cortex from fetal and neonatal rabbits (from 4–5 days preterm to 4 days of age) shows results comparable with maternal renal cortex during in vitro stimulation of the 2,200 ×
g pellet with parathyroid hormone (PTH) at 20 μg/ml. Incubation with sodium fluoride (10 mM), a nonspecific potent stimulator of adenyl cyclase, resulted in comparable increases in both the
fetal and the maternal renal cortex. Glucagon, prostaglandin E1, and vasopressin, all at 20 μg/ml, stimulate adenyl cyclase to a lesser extent than PTH. Homogenates of full term neonatal
rabbits and maternal renal cortex show comparable phosphodiesterase enzyme levels with or without 0.04 M imidazole. These data show that in fetal and early neonatal renal cortex there is no
developmental adenyl cyclase responsiveness to PTH. Similarly, phosphodiesterase is present equally in term and maternal rabbit renal cortex.
Speculation: A maturational response of adenosine 3′,5′-monophosphate (cyclic AMP) in urine to PTH has been previously suggested in the human full term neonate. This change in responsiveness
may not be due to a defect in the PTH hormone receptor or the adenyl cyclase enzyme of the proximal renal tubule. Other causes, such as impaired proximal tubular transport of cyclic AMP,
may account for this maturational response.
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