Developmental regulation of Na, K-ATPase in rat lung

Ingbar, David H.; Weeks, C. B.; Gilmore-Hebert, Maureen; Jacobsen, Einar; Duvick, S.; Dowin, R.; Savik, S. K.; Jamieson, J. D.

doi:10.1152/ajplung.1996.270.4.l619

Cited by 30 publications

(27 citation statements)

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“…Consequently, more ␤-adrenoceptors and higher ␤-adrenoceptor stimulation may lead to increased Na ϩ and fluid transport. The molecular mechanisms for this has been suggested to be stimulation of the apically located amiloride-sensitive ENaC (10,18,19,21,31,37,48) and increased expression and activity of basolateral Na-KATPases (6,23,48). Previously, we found significant increases in ENaC and Na-K-ATPase expression after IL-1␤ administration at both 61 and 68 days gestation (48).…”

Section: Discussionmentioning

confidence: 64%

“…Lung fluid absorption occurs secondarily to transepithelial Na ϩ absorption (3,5,8,17,22,31,35,37,45,48,49) and is driven by basolateral Na-K-ATPases (16,23) and apical epithelial sodium channels (19,22,30,31). Fluid absorption occurs in near-term lungs (6,17,35,37,45) and is induced/ stimulated by cortisol and triiodothyronine (2,20,48) and labor-released epinephrine (17,35,45).…”

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confidence: 99%

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Oxytocin-induced labor augments IL-1β-stimulated lung fluid absorption in fetal guinea pig lungs

Nair¹,

Li²,

Bhattacharjee³

et al. 2005

American Journal of Physiology-Lung Cellular and Molecular Phys

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-We tested the hypothesis that oxytocin-induced labor augmented IL-1␤-induced/ -stimulated lung fluid absorption in preterm guinea pig fetuses. IL-1␤ was administered subcutaneously daily to timed-pregnant guinea pigs for 3 days with and without simultaneous cortisol synthesis inhibition by metyrapone. At day 3, oxytocin was administered, and fetuses were delivered by abdominal hysterotomy at 61 and by oxytocin-induced birth at 68 days gestation. Delivered fetuses were instilled with isosmolar 5% albumin into the lungs, and lung fluid movement was measured over 1 h by mass balance. Lung fluid absorption was induced in 61-day and stimulated in 68-day gestation lungs by IL-1␤. Labor induction by oxytocin augmented IL-1␤-induced/-stimulated lung fluid absorption. Metyrapone pretreatment did not affect oxytocin-induced/-stimulated lung fluid absorption, while completely blocking IL-1␤-induced/-stimulated fluid absorption. Fetal lung fluid absorption, when present, was always propranolol and amiloride sensitive, suggesting that ␤-adrenoceptor stimulation and amiloridesensitive sodium channels were critical for fluid absorption. Epithelial sodium channel and Na-K-ATPase subunit expressions were both increased by IL-1␤, but not further by oxytocin. Our results indicate that IL-1␤ release into the maternal blood circulation positively affects lung maturation due to the IL-1␤-induced release of cortisol and thus prepares the lungs for the epinephrine surge associated with labor.␤-adrenoceptors; cortisol; epinephrine; prenatal lung development; sodium transport CYTOKINES, SUCH AS INTERLEUKIN-1 (IL-1), can be important during pregnancy, because IL-1 has been detected in the placenta and amniotic fluid (12,44). In this regard, interleukins have been proposed as a signal for parturition onset, as cytokines can stimulate prostaglandin biosynthesis (41). During normal pregnancies, IL-1 is present in the amniotic fluid in low concentrations, but during preterm labor much higher amniotic fluid IL-1 concentrations are present (44). Intrauterine infection/inflammation may further elevate cytokine levels, the highest activity being attributable to IL-1␤ (44). Many prematurely born infants suffer from fetal infection and/or respiratory distress syndrome (RDS), both of which are important reasons for mortality of premature babies. Recent human data suggest that ion transport abnormalities across lung epithelial cells, i.e., an incomplete transition of lung fluid secretion to lung fluid absorption, can contribute to RDS development (1). Factors accelerating ion transport across alveolar cells may thus have benefits for the resolution of RDS. Recent experimental data have suggested that proinflammatory cytokines could also promote lung maturation (9,14,26,47). IL-1␣ increased mRNA surfactant protein expression and improved lung compliance in fetal rabbits (9). IL-1␣ also improved postnatal lung function with increased surfactant pool size without eliciting systemic inflammatory responses in lambs (14, 47). We recently reported that IL-...

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Section: Discussionmentioning

confidence: 64%

mentioning

confidence: 99%

Oxytocin-induced labor augments IL-1β-stimulated lung fluid absorption in fetal guinea pig lungs

Nair¹,

Li²,

Bhattacharjee³

et al. 2005

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…Although low ENaC mRNA levels were detected in rat fetuses of any gestational age (17), the prenatal increase of ENaC and Na,K-ATPase subunit expression was not observed before 19 -22 d of gestation, i.e. shortly before term birth at 22 d (17)(18)(19)(20). If the ontogeny of ENaC and Na,K-ATPase follows a similar pattern in human fetuses and preterm infants (21), the participants of our study would have been born long before the prenatal increase of ENaC and Na,K-ATPase subunit expression (22).…”

Section: Discussionmentioning

confidence: 90%

Amiloride-Sensitive Nasal Potential Difference Is Not Changed by Estradiol and Progesterone Replacement But Relates to BPD or Death in a Randomized Trial on Preterm Infants

et al. 2006

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Postnatal replacement of placental estradiol (E2) and progesterone (P) in preterm infants may improve lung function, possibly mediated through enhanced epithelial Na ϩ transport and alveolar fluid clearance. Preterm infants of Ͻ29 wk gestational age and Ͻ1000 g birth weight requiring mechanical ventilation within 12 h of birth were randomized to receive either 2.5 mg/kg E2 and 22.5 mg/kg P per day (E2/P), or vehicle placebo. Epithelial Na ϩ transport was assessed in 29 infants by measuring total nasal potential difference (NPD) and amiloride-sensitive NPD (ASNPD) on postnatal days of life 1, 3, 5, and 7, and mean values of all four measurements were calculated. Bronchopulmonary dysplasia (BPD) was defined as need for supplemental oxygen (goal SaO 2 90%) or mechanical ventilation at 36 wk corrected postmenstrual age. Mean ASNPD was Ϫ6.5 Ϯ 2.8 mV in infants receiving E2/P and Ϫ6.1 Ϯ 2.6 mV in infants receiving placebo (not significant). NPD was Ϫ10.6 Ϯ 3.8 mV and Ϫ10.7 Ϯ 3.6 mV, respectively. The ASNPD was significantly higher in infants surviving without BPD (Ϫ7.1 Ϯ 2.5 mV) than in infants developing BPD or not surviving (Ϫ5.2 Ϯ 2.4 mV). In conclusion, ASNPD is not changed by postnatal replacement of E2 and P. A steady improvement of preterm infant survival and respiratory morbidity was observed from 1990 until 1998 and was attributed to the introduction of exogenous surfactant and antenatal steroids (1). Thereafter, the frequencies of adverse outcomes showed a plateau. Many infants still develop respiratory distress syndrome (RDS) despite surfactant administration, and the incidence of BPD appeared to be increasing again recently (1). Novel therapies are needed to further reduce respiratory morbidity.Aside from producing surfactant, alveolar type II cells (AT2) are responsible for postnatal clearance of excess fluid from the airspaces by moving Na ϩ ions from the apical to the basolateral side, which creates a measurable electrochemical gradient as well as an osmotic gradient driving water movement in the same direction (2). The importance of this process is best demonstrated by mice lacking the pore-forming ␣-subunit of the epithelial Na ϩ channel (ENaC), which invariably die from pulmonary edema and respiratory failure within 40 h of birth (3). Infant RDS may in part be caused by inadequate epithelial Na ϩ transport (4). Furthermore, survival of adults suffering from acute RDS has been related to alveolar fluid clearance (5). Lung water content (6) and epithelial ion transport (7) have also been related to pulmonary compliance.Epithelial ion transport is inaccessible inside the lungs of intact subjects, but the transport mechanisms are expressed in all respiratory epithelia including the trachea and nose. The resulting electrochemical gradient can be readily measured at the nasal epithelium and is known as the NPD. The contribution of ENaC-dependent Na ϩ transport to total NPD can be determined by the ASNPD, defined as the decrease in potential following the application of the ENaC blocker amiloride....

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“…The Na,K-ATPase isoforms are expressed in a tissue-and development-specific fashion and are believed to be distinct in both function and modes of regulation (3). The ␣ 1 isoform is predominant in most epithelia, including rat lung (4). The Na,K-ATPase activity is differentially regulated in a hormone-and tissue-specific fashion (1).…”

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confidence: 99%

3,3′,5-Triiodo-l-thyronine Up-regulation of Na,K-ATPase Activity and Cell Surface Expression in Alveolar Epithelial Cells Is Src Kinase- and Phosphoinositide 3-Kinase-dependent

Lei

Mariash

Ingbar

2004

Journal of Biological Chemistry

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Developmental regulation of Na, K-ATPase in rat lung

Cited by 30 publications

References 0 publications

Oxytocin-induced labor augments IL-1β-stimulated lung fluid absorption in fetal guinea pig lungs

Oxytocin-induced labor augments IL-1β-stimulated lung fluid absorption in fetal guinea pig lungs

Amiloride-Sensitive Nasal Potential Difference Is Not Changed by Estradiol and Progesterone Replacement But Relates to BPD or Death in a Randomized Trial on Preterm Infants

3,3′,5-Triiodo-l-thyronine Up-regulation of Na,K-ATPase Activity and Cell Surface Expression in Alveolar Epithelial Cells Is Src Kinase- and Phosphoinositide 3-Kinase-dependent

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