Euhydric hypercapnia increases vasoreactivity of rat pulmonary arteries via HCO 3- transport and depolarisation

Citations of this article
Mendeley users who have this article in their library.


To examine whether altered PCO 2 or HCO 3- at normal pH potentiate agonist-induced vasoconstriction of small pulmonary arteries, and if so to determine the mechanism. Small intrapulmonary arteries (IPA) from rats were mounted on a myograph and PGF 2α (3 μM)-induced tension recorded before and 40 min after replacing normal bath solution (5% CO 2, 24 mM [HCO 3-], pH 7.4) with one containing either normal [HCO 3-] (24 mM) gassed with 10% CO 2 (pH 7.12; hypercapnic acidosis) or high [HCO 3-] (48 mM) gassed with 10% CO 2 (pH 7.4; euhydric hypercapnia). Hypercapnic acidosis had no significant effect on the response of IPA to PGF 2α. Euhydric hypercapnia however caused a substantial ∼5.5-fold potentiation of the response (n=17, p<0.001) in the majority of preparations, whilst 20% of IPA (11 of 58) developed a slow spontaneous vasoconstriction after ∼20 min. No equivalent responses to euhydric hypercapnia were observed in either mesenteric or renal arteries. Both the potentiation of PGF 2α-induced vasoconstriction and the spontaneous vasoconstriction in IPA were inhibited by the L-type channel blocker diltiazem (10 μM). The potentiation was also suppressed by DIDS, an inhibitor of anion transporters, removal of extracellular Na +, and anthracene-9-carboxylic acid (A9C; 200 μM), reported to inhibit Ca 2+-activated Cl - channels. Inhibition of nitric oxide synthase with l-NAME (100 μM) did not prevent potentiation. Depolarisation with 20 mM [K +] mimicked the effect of euhydric hypercapnia in that it also potentiated the response to PGF 2α (>sixfold, n=6). Euhydric hypercapnia increases vasoreactivity of IPA, but not mesenteric or renal arteries, via a mechanism involving Na +-dependent HCO 3- transport, activation of Ca 2+-dependent Cl - channels, and subsequent depolarisation. These results may have consequences for patients with CO 2-retaining chronic respiratory disease where plasma [HCO 3-] is raised following renal compensation, and could explain the increased propensity to pulmonary hypertension and increased mortality in such patients. © 2004 European Society of Cardiology. Published by Elsevier B.V. All rights reserved.




Vaňková, M., Snetkov, V. A., Knock, G. A., Aaronson, P. I., & Ward, J. P. T. (2005). Euhydric hypercapnia increases vasoreactivity of rat pulmonary arteries via HCO 3- transport and depolarisation. Cardiovascular Research, 65(2), 505–512.

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free