Dobutamine Increases Alveolar Liquid Clearance in Ventilated Rats by Beta-2 Receptor Stimulation

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Abstract
Although it is well known that beta-adrenergic agonist stimulation increases alveolar epithelial sodium and fluid transport, it is not known whether the beta-1 or the beta-2 receptor mediates this effect. Two clinically relevant beta-adrenergic agonists, dopamine (beta-1 agonist) and dobutamine (beta-1 and beta-2 agonist) were used to define the contribution of these two beta-receptors to beta-adrenergic stimulated fluid clearance from the air spaces of the lungs. Alveolar fluid clearance was measured in anesthetized, ventilated rats over one hour after instilling an isosmolar 5% albumin solution in Ringer's lactate with 3 μ Ci 125I-albumin. The concentrations of the labeled and unlabeled albumin were used to quantify alveolar liquid clearance. Dopamine, whether given intra-alveolar (10− 4 M) or intravenously (5–10 μ g/kg/min), had no effect. However, both intra-alveolar (10− 4 M) and intravenous (5 μ g/kg/min) dobutamine increased alveolar liquid clearance by approximately 50% over one hour compared to controls. ICI 118,551, a potent and specific beta-2 antagonist, blocked the effect of dobutamine. The dobutamine effect was blocked by amiloride (10− 3 M), an inhibitor of sodium uptake. In summary, the beta-2 receptor mediates beta-adrenergic stimulation of alveolar epithelial sodium and fluid transport.