131I-metaiodobenzylguanidine uptake in the isolated rat lung: a potential marker of endothelial cell function.

The pulmonary vascular endothelial cell plays an important role in the uptake of circulating biogenic amines. In cultured adrenomedullary cells, metaiodobenzylguanidine (MIBG) and norepinephrine (NE) are taken up by the same sodium-dependent active transport system. To examine whether a similar process occurs in the lung, the mechanism of single pass 131I-MIBG accumulation was studied in rat lungs perfused with a Krebs-Ringer bicarbonate buffer containing 4.5% bovine albumin. MIBG lung accumulation was measured as the percent extraction per g of lung tissue. In control experiments the extraction was 19.7 +/- 2.3%/g (n = 38) using a perfusate containing 0.01 microM MIBG. MIBG accumulation was significantly depressed (% decrease from control) by: cold media at 4 degrees C (84%), 0.5 mM ouabain (67%), 10 microM imipramine (70%), 0.7 microM serotonin (22%) and 40 mM K+ (48%). Pulmonary uptake of MIBG was characterized by Michaelis-Menten kinetics (Km = 0.92 x 10(-6) M and Vmax = 2.09 x 10(-9) moles/g per min). The addition of NE (0.5 microM) also altered MIBG uptake such that the Km and Vmax became 0.52 x 10(-6) M and 0.93 x 10(-9) moles/g per min, respectively. The results indicate that MIBG accumulation in the lung involves sodium-dependent, energy-requiring, active transport mechanisms similar to those known to exist for norepinephrine, and suggest that MIBG may be useful as a marker of pulmonary endothelial cell function.