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Renal Receptor Linked to Kidney Function at Birth

Mineralocorticoid receptor low at birth; mediates effects of aldosterone

MONDAY, June 8 (HealthDay News) -- The levels of renal mineralocorticoid receptors are low at birth, even though mineralocorticoid receptor-mediated aldosterone levels are high, which may explain why newborns have an impaired capacity to regulate water and sodium homeostasis, according to a study published online May 28 in Endocrinology.

Laetitia Martinerie, M.D., from University Paris-Sud 11 in Le Kremlin-Bicetre, France, and colleagues measured aldosterone and renin levels in umbilical cord blood from healthy newborns, and analyzed the expression of mineralocorticoid receptors during renal development in mice and humans.

The researchers found that aldosterone and renin levels were high at birth. Mineralocorticoid receptors were expressed at 15 to 24 weeks gestation in human kidneys but were undetectable during late gestation and in neonates. Similar results were observed during renal development in mice. The cyclical changes in mineralocorticoid receptor levels were associated with changes in 11β-hydroxysteroid dehydrogenase type 2 and the epithelial sodium channel α-subunit. Conversely, the authors note, glucocorticoid and vasopressin receptors, and aquaporin 2 developed in a sustained, progressive manner during maturation of the kidneys.

"Our study provides first evidence for a low renal mineralocorticoid receptor expression level at birth, despite high aldosterone levels, which could account for compromised postnatal sodium handling," Martinerie and colleagues conclude.

An author of the study reported a financial relationship with the pharmaceutical industry.

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