Received January 25, 2007
Revised March 21, 2007
Accepted after revision May 8, 2007

Daniel Hodyc ^1*, Michal norek ¹, Tomá Brtnick ¹, Jan Herget ¹

¹ Department of Physiology, Charles University in Prague, 2nd Medical School, Prague

^* To whom correspondence should be addressed. E-mail: daniel.hodyc{at}lfmotol.cuni.cz.

	Abstract

Hypoxic pulmonary vasoconstriction (HPV), as an important physiological mechanism, is regulated by changes in the production of and interactions among reactive oxygen species (ROS). However, there is a controversy as to whether HPV is mediated by an increase or a decrease in ROS production. Also, the role of NO in HPV remains unclear. The aim of this study was to investigate whether the inhibition of HPV by the antioxidant tempol was depended on the concentration of NO, and how its effect was influenced by increased basal pulmonary vascular tone. In isolated rat lungs we measured vasoconstrictor responses to acute ventilatory hypoxia before and after administration of tempol during perfusion with or without L-NAME. We found that tempol abolished HPV independently of NO production. When we increased basal vascular tone by K+ - induced depolarization, we also found that tempol completely inhibited HPV. Our results indicate that inhibition of HPV by the SOD mimetic tempol does not depend on either NO production or a decrease in basal vascular tone.

Key Words: Free radical, Hypoxia, Pulmonary circulation

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				J. P. T. Ward Curiouser and curiouser: the perplexing conundrum of reactive oxygen species and hypoxic pulmonary vasoconstriction Exp Physiol, September 1, 2007; 92(5): 819 - 820. [Full Text] [PDF]