In both inner medullary collecting duct (IMCD) cells and alveolar cells stimulation of β2 adrenergic receptors results in renal tubular and alveolar Na+ reabsorption. We sought to explore the relationship between Na+ composition of urine and plasma to that of exhaled breath condensate (EBC, a surrogate for airway surface liquid composition) following β‐agonist administration. We recruited 17 healthy subjects (age=27±9yrs, ht.=170±8cm, wt.=68±12kg, BMI=24±4kg/m2, mean±SD) to complete two visits with administration of either nebulized β‐agonist (albuterol, 2.5mg) or nebulized saline with measures of EBC, plasma, and urine Na+ at baseline and 90 minutes post in a blind crossover design. At baseline there was no relationship between EBC Na+ and urine Na+ nor in urine Na+ and plasma Na+, but there was a relationship between EBC Na+ and plasma Na+ (r=0.35, 1‐tailed p=0.034). Albuterol resulted in a small but insignificant reduction in EBC Na+ (baseline=2.52±1.5, 90min post=2.17±1.4mmol/l), but no change in plasma or urine Na+. Saline resulted in no change in EBC Na+ (baseline=1.96±0.4, 90min post=1.91±0.5) or plasma or urine Na+. These results suggest a relationship between plasma Na+ and EBC Na+, but not between EBC Na+ and urine Na+ likely due to multiple regulatory pathways for renal Na+ handling independent of IMCD cells that constitute the majority of renal Na+ reabsorption and are not also present in the lung.