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Endothelial NO formation does not control myocardial O₂ consumption in mouse heart

¹Institut für Herz- und Kreislaufphysiologie, Heinrich-Heine-Universität Düsseldorf, 40001 Düsseldorf, Germany

Submitted 18 September 2002 ; accepted in final form 5 March 2003

To test whether endothelium-derived nitric oxide (NO) regulates mitochondrial respiration, NO was pharmacologically modulated in isolated mouse hearts, which were perfused at constant flow to sensitively detect small changes in myocardial O₂ consumption (MO₂). Stimulation of NO formation by 10 µM bradykinin (BK) increased coronary venous nitrite release fivefold to 58 ± 33 nM (n = 17). Vasodilatation by BK, adenosine (1 µM), or papaverine (10 µM) decreased perfusion pressure, left ventricular developed pressure (LVDP), and MO₂. In the presence of adenosine-induced vasodilatation, stimulation of endothelial NO synthesis by BK had no effect on LVDP and MO₂. Also, inhibition of NO formation by N^G-monomethyl-L-arginine (L-NMMA, 100 µM) did not significantly alter LVDP and MO₂. Similarly, intracoronary infusion of authentic NO ≤2 µM did not influence LVDP or MO₂ (-1 ± 1%). Only when NO was >2 µM were contractile dysfunction and MO₂ reduction observed. Because BK-induced stimulation of endothelial NO formation and basal NO are not sufficient to impair MO₂ in the saline-perfused mouse heart, a tonic control of the respiratory chain by endothelial NO is difficult to conceive.

nitrite; bradykinin; nitric oxide synthase inhibition

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