Local and Peripheral Plasma Endothelin-1 in Pulmonary Hypertension Secondary to Chronic Obstructive Pulmonary Disease

Endothelin-1 (ET-1) has been described to have crucial effects in the initiation and evolution of pulmonary hypertension (PH) secondary to cardiac disorders. However, the precise role of ET-1 in PH induced by chronic obstructive pulmonary disease (COPD) is not yet clear. The objective of this cross-sectional study was to determine the local and peripheral plasma ET-1 profile of COPD patients with or without PH. Twenty-six COPD patients with clinical and/or laboratory findings suspicious of PH, and 20 healthy smoker volunteers constituted the study population. Patients were allocated to PH (n = 17) and non-PH (n = 9) groups according to their pulmonary artery pressures determined by right-heart catheterization. Plasma ET-1 samples, obtained from the main pulmonary artery (mixed venous blood) and peripheral blood (radial artery and brachial vein), were assessed by radioimmunoassay. Brachial vein ET-1 levels were within normal ranges in PH (2.7 +/- 0.5 pg/ml) and non-PH (3.2 +/- 0. 7 pg/ml) COPD patients compared with that of the controls (4.4 +/- 0. 1 pg/ml). Likewise, radial artery ET-1 levels in PH (3.3 +/- 0.7 pg/ml) and non-PH (2.9 +/- 0.8 pg/ml) groups, and in controls (3.4 +/- 1.1 pg/ml) were also comparable. The pulmonary artery ET-1 concentration of the PH group (13.6 +/- 3.7 pg/ml) was higher than that of the non-PH group (2.2 +/- 0.4 pg/ml) and that of the peripheral blood levels of controls. Elevated pulmonary artery ET-1 in the PH group was inversely correlated only with PaO2 levels. These results could be taken as an evidence of a local role of ET-1 in COPD-induced PH, but it remains to be clarified whether ET-1 is a marker or a mediator of PH in COPD.