Effects of thyroid hormone on the neonatal renal cortical Na+/H+ antiporter

Abstract

The neonatal proximal tubule has a lower rate of bicarbonate absorption than that of adults. This is due, in part, to a lower rate of apical membrane Na+/H+ antiporter activity. The purpose of these studies was to examine if thyroid hormone could be a factor in the maturational increase in Na+/H+ antiporter activity. Hypothyroid (0.01% propylthiouracil in drinking water starting at day 14 gestation and throughout the postnatal period), euthyroid, and hyperthyroid (intraperitoneal triiodothyronine, 10 micrograms/100 g body wt, once daily on days 17 to 20 of postnatal life) rats were all studied at 21 days of life. Renal cortical brush border Na+/H+ antiporter activity was 453 +/- 24, 527 +/- 30 and 608 +/- 25 pmol/mg protein in the hypothyroid, euthyroid and hyperthyroid groups, respectively (P < 0.001). Hyperthyroid neonates had approximately twofold greater renal cortical NHE-3 mRNA abundance than euthyroid and hypothyroid neonates (P < 0.05). Brush border membrane NHE-3 protein abundance in hypothyroid and hyperthyroid neonates was one-third and twofold that of euthyroid 21-day-old rats, respectively (P < 0.001). These data are consistent with a potential role of thyroid hormone in the postnatal increase in Na+/H+ antiporter activity.

Ontogeny of Na+/H+ Antiporter Activity in Rat Proximal Convoluted Tubules

“…The cortex was dissected and then homogenized with 20 strokes with a polytetrafluoroethylene-glass homogenizer at 4°C. BBMV were then isolated by differential centrifugation and magnesium precipitation as previously described (21). The final BBMV fraction was resuspended in isolation buffer.…”

“…BBMV protein (50 g/ lane) was denatured and separated on a 7.5% polyacrylamide gel as previously described (21,22). The proteins were transferred to polyvinylidene difluoride membrane overnight at 140 mA at 4°C.…”

The Thyroid and the Kidney: A Complex Interplay in Health and Disease

“…However, there are anecdotal reports that long-term use of angiotensin converting enzyme (ACE) inhibitors or AT II receptor blockers (ARBs) did not regress renal hypertrophy in hyperthyroid animals (31,32). Thyroid hormone participates in the development of many co-transport systems in the renal tubule including renal Na + co-transported phosphate, cortical Na + /H + exchanger (NHE), and Na + -K + adenosine-triphosphatase (33)(34)(35)(36)(37). Notably, Wijkhuisen et al (38) suggested that thyroid hormone regulates the development of several energy metabolism enzymes of proximal convoluted tubule of perinatal rats such us the enzyme 3-ketoacidCoA transferase, citrate synthase and carnitine acetyltransferase.…”

Different effects of maternal parity, cold exposure and nutrient restriction in late pregnancy on the abundance of mitochondrial proteins in the kidney, liver and lung of postnatal sheep

“…In contrast, thyroid hormones are raised in cold-exposed mothers (Symonds et al 1988a) and decrease with parity (Tasende et al 2002), differences that are maintained through lactation (Symonds et al 1990). Hypothyroidism has been shown to delay kidney maturation after birth, resulting in decreased renal cortical Na C /H C transporter activity and brush border membrane NHE-3 protein abundance (Baum et al 1998), blunted maturational increase in both Na C /H C and Cl K /OH K exchange activity (Shah et al 2000), and lower rates of sodiumdependent proton secretion (Gupta et al 2004). Differences in maternal and neonatal plasma thyroid hormone concentrations may, therefore, contribute to the maternal effects on mitochondrial protein abundance in the kidney we have found that appear to be confined to the tubular region.…”