Abstract
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 KCl under control conditions (5% CO 2–95% air). IH was achieved by switching to a modified PSS (isosmotic substitution of NaHCO 3 for NaCl), equilibrated with 10% CO 2 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.
Published Version
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