Calcium-dependent Stimulation Of Alveolar Fluid Clearance In Near Term Fetal Guinea Pigs
Biochemistry & Molecular Biology; Cell Biology; Life Sciences & Biomedicine - Other; Topics
Folkesson H G; Ye X; Norlin A
Faseb Journal
2001
2001-03
Journal Article or Conference Abstract Publication
n/a
Contribution of amiloride-insensitive pathways to alveolar fluid clearance in adult rats
anesthetized sheep; cation channels; channels; conductance; cyclic nucleotide-gated cation channels; dibutyryl-guanosine-3'5'-cyclic monophosphate; distal lung; epithelial na+ channel; epithelial sodium ion; guinea-pigs; isoproterenol; l-cis-diltiazem; lung liquid clearance; Physiology; protein clearance; sodium transport; Sport Sciences; terbutaline
The contributions of amiloride-sensitive and -insensitive fractions of alveolar fluid clearance in adult ventilated rats were studied under control conditions and after beta -adrenergic stimulation. Rats were instilled with a 5% albumin solution containing terbutaline (10(-4) M) or dibutyryl-cGMP (DBcGMP; 10-4 M) with or without the cyclic nucleotide-gated cation channel inhibitor l-cis-diltiazem (10(-3) M) and/or amiloride (10-3 M). Alveolar fluid clearance over 1 h was 18 +/- 2% in controls. In controls, amiloride inhibited 46 +/- 15% of alveolar fluid clearance, whereas l-cis-diltiazem had no inhibitory effect. Terbutaline and DBcGMP stimulated alveolar fluid clearance by 85 +/- 3 and 36 +/- 5%, respectively. Amiloride and l-cis-diltiazem inhibited nearly equal fractions of terbutaline-stimulated alveolar fluid clearance when given alone. Amiloride and l-cis-diltiazem given together inhibited a significantly larger fraction of alveolar fluid clearance in terbutaline-stimulated rats and in DBcGMP-stimulated rats. Based on these data, tertbutaline stimulation recruited both amiloride-sensitive and E-cis-diltiazem-sensitive pathways. In contrast, DBcGMP mainly recruited l-cis-diltiazem-sensitive pathways. Therefore, the amiloride-insensitive fraction of Nat-driven alveolar fluid clearance may be partly mediated through cyclic nucleotide-gated cation channels and activated by an increase in intracellular cGMP.
Norlin A; Lu L N; Guggino S E; Matthay M A; Folkesson H G
Journal of Applied Physiology
2001
2001-04
Journal Article
<a href="http://doi.org/10.1152/jappl.2001.90.4.1489" target="_blank" rel="noreferrer noopener">10.1152/jappl.2001.90.4.1489</a>
Alveolar epithelial ion and fluid transport - Ca2(+)-dependent stimulation of alveolar fluid clearance in near-term fetal guinea pigs
adrenaline; agonist; amiloride; birth; blood-flow; cation; channel; distal lung epithelium; expression; lamb; liquid; oxytocin-induced preterm labor; Physiology; protein clearance; Respiratory System; sodium transport; surfactant secretion
We investigated the importance of changes in intracellular Ca2+ concentration ([Ca2+](i)) for amiloride-sensitive alveolar fluid clearance (AFC) in late-gestational guinea pigs. Fetal guinea pigs of 61, 68, and 69 days (term) gestation were investigated under normal conditions and after oxytocin-induced preterm labor. AFC or alveolar fluid secretion was measured using an impermeable tracer technique. At 61 days gestation there was net secretion of fluid into the lungs, and at birth the lungs cleared 49 +/- 7% of the instilled fluid volume over 1 h. Induction of preterm labor with oxytocin induced AFC at 61 days gestation. When present, AFC was inhibited or reversed to net fluid secretion by amiloride (10(-3) M). Inhibition of membrane Ca2+ channels by verapamil (10(-4) M) or depletion of intracellular Ca2+ by thapsigargin (10(-5) M) reduced AFC when net AFC was evident. Amiloride lacked an inhibitory effect on AFC when instilled with verapamil or thapsigargin. The results indicate that AFC via amiloride-sensitive pathways develops during late gestation, and that inducing preterm labor precociously may activate such pathways. Our results suggest that Ca2+ may act as a second messenger in mediating catecholamine-stimulated AFC.
Norlin A; Folkesson H G
American Journal of Physiology-Lung Cellular and Molecular Physiology
2002
2002-04
Journal Article
<a href="http://doi.org/10.1152/ajplung.00417.2000" target="_blank" rel="noreferrer noopener">10.1152/ajplung.00417.2000</a>
Alveolar fluid clearance in late-gestational guinea pigs after labor induction: mechanisms and regulation
absorption; adrenaline; alveolar epithelium; beta-adrenergic stimulation; birth; catecholamines; developmental-changes; distress syndrome; epinephrine; fetal sheep; infant respiratory; lung liquid clearance; newborn rabbits; Physiology; prenatal development; Respiratory System; sodium transport; transport; ventilated rats
We tested the hypothesis that labor-induced epinephrine release would stimulate alveolar fluid clearance in preterm fetuses. Preterm fetuses were obtained by cesarean section from timed-pregnant guinea pigs at 61-69 days postconception. Fetal guinea pigs were euthanized and placed on continuous positive airway pressure oxygenation, and an isosmolar 5% albumin solution was instilled. Alveolar fluid clearance was measured over 1 h. The fetal lung began to absorb fluid at 64-66 days postconception, and at birth, alveolar fluid clearance quadrupled. Baseline alveolar fluid clearance when present was sensitive to propranolol inhibition and depended on beta -adrenergic stimulation. Measurements of plasma epinephrine in fetal animals confirmed high epinephrine levels in 66- to 69-day postconception fetuses. Prenatal alveolar fluid clearance when present was highly amiloride sensitive, suggesting that amiloride-sensitive Na+ channels were critical. Oxytocin-induced labor initiated an amiloride- and propranolol-sensitive net alveolar fluid clearance in 61-day-gestation animals. Moreover, oxytocin induced significant epinephrine release in all fetuses. These results have clinical implications for infants delivered by cesarean section before the onset of labor. Use of pharmacological agents to induce labor may reduce the occurrence and severity of perinatal respiratory distress.
Norlin A; Folkesson H G
American Journal of Physiology-Lung Cellular and Molecular Physiology
2001
2001-04
Journal Article
<a href="http://doi.org/10.1152/ajplung.2001.280.4.l606" target="_blank" rel="noreferrer noopener">10.1152/ajplung.2001.280.4.l606</a>