• Ives Hubloue, Benoît Rondelet, François Kerbaul, Dominique Biarent, Guiti Malekzadeh Milani, Michel Staroukine, Pierre Bergmann, Robert Naeije, and Marc Leeman.
• Department of Intensive Care Medicine, Akademisch Ziekenhuis VUB, and Laboratory of Physiology, Faculty of Medicine, Erasme Campus of the Free University of Brussels, Brussels, Belgium. ives.hubloue@az.vub.ac.be
• Crit Care. 2004 Aug 1; 8 (4): R163-71.

IntroductionThe role played by several vasoactive mediators that are synthesized and released by the pulmonary vascular endothelium in the regulation of hypoxic pulmonary vasoconstriction (HPV) remains unclear. As a potent vasoconstrictor, angiotensin II could be involved. We tested the hypothesis that angiotensin-converting enzyme inhibition by enalaprilat and type 1 angiotensin II receptor blockade by candesartan would inhibit HPV.MethodsHPV was evaluated in anaesthetized dogs, with an intact pulmonary circulation, by examining the increase in the Ppa-Ppao gradient (mean pulmonary artery pressure minus occluded pulmonary artery pressure) that occurred in response to hypoxia (inspiratory oxygen fraction of 0.1) at constant pulmonary blood flow. Plasma renin activity and angiotensin II immunoreactivity were measured to determine whether activation or inhibition of the renin-angiotensin system was present.ResultsAdministration of enalaprilat and candesartan did not affect the Ppa-Ppao gradient at baseline or during hypoxia. Plasma renin activity and angiotensin II immunoreactivity increased during hypoxia, and subsequent measurements were consistent with effective angiotensin-converting enzyme inhibition after administration of enalaprilat, and with angiotensin receptor blockade after administration of candesartan.ConclusionThese results suggest that, although the renin-angiotensin system was activated in hypoxia, angiotensin II is not normally involved in mediating acute HPV.

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