Hypercapnia-induced contraction in isolated pulmonary arteries is endothelium-dependent

It has been demonstrated previously that isohydric hypercapnia (IH) does not affect agonist-induced tension development in pulmonary arteries. The aim of the present study was to examine the effects of IH on depolarisation-induced, steady state tension in the isolated rat pulmonary artery. Rings were submaximally contracted with high KCI under control conditions (5% CO2-95% air). IH was achieved by switching to a modified PSS (isosmotic substitution of NaHCO3 for NaCl), equilibrated with 10% CO2 in air. On switching to IH, a significant increase in mean ( +/- SEM) tension (25.3 +/- 6.3% Tmax) was observed in endothelium intact rings (n = 6). Endothelial removal significantly reduced this response. Non-specific inhibition of nitric oxide synthase (NOS) isoenzymes (L-NAME, 10(-3) M) abolished the IH-induced increase in tension while inhibition of neuronal NOS (TRIM, 10(-5) M) was without effect. The relaxant response to the nitric oxide donor sodium nitroprusside was similar in IH and control conditions. These results suggest that IH caused an endothelium-dependent increase in depolarisation-induced tension by reducing NO production. (C) 2000 Elsevier Science B.V. All rights reserved.