It has been demonstrated previously that isohydric hypercapnia (IH) does no
t affect agonist-induced tension development in pulmonary arteries. The aim
of the present study was to examine the effects of IH on depolarisation-in
duced, steady state tension in the isolated rat pulmonary artery. Rings wer
e submaximally contracted with high KCI under control conditions (5% CO2-95
% air). IH was achieved by switching to a modified PSS (isosmotic substitut
ion 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 signi
ficantly reduced this response. Non-specific inhibition of nitric oxide syn
thase (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 e
ffect. The relaxant response to the nitric oxide donor sodium nitroprusside
was similar in IH and control conditions. These results suggest that IH ca
used an endothelium-dependent increase in depolarisation-induced tension by
reducing NO production. (C) 2000 Elsevier Science B.V. All rights reserved
.