The hypothesis that nitrite is converted to nitric oxide in the red blood cell (RBC) perfused coronary circulation of rainbow trout was tested. A Langedorff-type isolated heart preparation was used, which was perfused with trout physiological saline or RBCs suspended in saline (Hct ~6%), at various input Po₂ levels. Coronary flow and pressure, and input and output Po₂, pH, Hct, Hb, metHb and nitrite were measured. Nitric oxide was recorded in the atrial effluent of the preparation. RBC perfusion established a strong linear increase in myocardial O₂ consumption with coronary flow. Perfusion with saline under hypoxic conditions was associated with NO production. The nitric oxide synthase inhibitor L-NA obliterated this NO production and significantly decreased coronary flow, showing that the NO was of endothelial origin and that it was vasoactive. RBC perfusion at low Po₂ similarly caused an L-NA-inhibitable NO production. The change in NO production upon subsequent nitrite addition, in contrast, was not inhibited by L-NA. Nitrite entered trout erythrocytes independent of oxygenation degree. The O₂ saturation of RBCs showed a major decrease in the coronary circulation, and a concomitant nitrite entry and methaemoglobin increase suggested that deoxyHb-mediated reduction of nitrite to NO may have occurred. However, other possibilities (e.g. NO₂^- ? NO conversion in myocardial cells) cannot be excluded. The NO formation associated with nitrite was without effect on coronary flow, possibly because NO was produced after the resistance vessels.

REFERENCE

Jensen, F.B., Agnisola, C. 2005. J Exp Biol 208, 3665-3674.