Catecholamines increase lung edema clearance in rats with increased left at
rial pressure. J Appl Physiol 90: 1088-1094, 2001.-During hydrostatic pulmo
nary edema, active Na+ transport and alveolar fluid reabsorption are decrea
sed. Dopamine (DA) and isoproterenol (ISO) have been shown to increase acti
ve Na+ transport in rat lungs by upregulating Na+-K+-ATPase in the alveolar
epithelium. We studied the effects of DA and ISO in isolated rat lungs wit
h increased left atrial pressure (Pla = 15 cmH(2)O) compared with control r
ats with normal Pla (Pla = 0). Alveolar fluid reabsorption decreased from c
ontrol value of 0.51 +/- 0.02 to 0.27 +/- 0.02 ml/h when Pla was increased
to 15 cmH(2)O (P < 0.001). DA and ISO increased the alveolar fluid reabsorp
tion back to control levels. Treatment with the D-1 antagonist SCH-23390 in
hibited the stimulatory effects of DA (0.30 +/- 0.02 ml/h), whereas fenoldo
pam, a specific D-1- receptor agonist, increased alveolar fluid reabsorptio
n in rats exposed to Pla of 15 cmH(2)O (0.47 +/- 0.04 ml/h). Propranolol, a
<beta>-adrenergic-receptor antagonist, blocked the stimulatory effects of
ISO; however, it did not affect alveolar fluid reabsorption in control or D
A-treated rats. Amiloride (a Na+ channel blocker) and ouabain (a Na+-K+-ATP
ase inhibitor), either alone or together, inhibited the stimulatory effects
of DA. Colchicine, which disrupts the cellular microtubular transport of i
on-transporting proteins to the plasma membrane, inhibited the stimulatory
effects of DA, whereas the isomer beta -lumicolchicine did not block the st
imulatory effects of DA. These data suggest that DA and ISO increase alveol
ar fluid reabsorption in a model of increased Pla by regulating active Natransport in rat alveolar epithelium. The effects of DA and ISO are mediate
d by the activation of dopaminergic D-1 receptors and the beta -adrenergic
receptors, respectively.