The influence of the transmembrane sodium gradient on the responses of pulmonary arteries to decreases in oxygen tension.

A Na/Ca exchange system has been demonstrated in systemic vascular smooth muscle and has been suggested as a mechanism for the entry and extrusion of Ca2+. Using isolated rings of bovine intrapulmonary arteries, we sought to determine whether a Na/Ca exchange mechanism is present in pulmonary vascular smooth muscle, and if so, whether it contributes to the modulation of vascular tone during hypoxia. Under both normoxic (PO2 greater than or equal to 120 mm Hg) and hypoxic (PO2 less than or equal to 40 mm Hg) conditions, the amplitude of the 40 mM K+ contraction was significantly (p less than 0.005) enhanced when most of the external Na+ was replaced with N-methylglucamine (NMG) (Na+ = 1.2 mM). The rate of contraction was also increased by replacing Na+ with NMG during normoxia (1.02 +/- 0.24 to 2.52 +/- 0.57 mg/mg weight/s, p less than 0.005) and hypoxia (1.72 +/- 0.74 to 4.08 +/- 1.63 mg/mg weight/s, p less than 0.05). Although the relaxation rate was slowed in the low Na+ media during normoxia (3.48 +/- 1.07 with Na+ versus 2.58 +/- 0.81 mg/mg weight/s with NMG, p less than 0.02), it was unaltered during hypoxia (3.15 +/- 0.90 with Na+ versus 2.95 +/- 0.83 mg/mg weight/s with NMG, p = 0.3). The ratio of relaxation rates in the normal and low Na+ media correlated with the perfusate PO2 (r = 0.76, p less than 0.001). During normoxia and hypoxia, inhibition of the Na+,K+ pump by strophanthidin, which increases intracellular [Na+], reversibly enhanced the amplitude of the K+ contraction, even when the voltage-gated channels were blocked with verapamil.(ABSTRACT TRUNCATED AT 250 WORDS)