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Recently, cytokines have been proposed to cause cellular injury by nitric oxide (NO.) mediated pathway and L-arginine has been proposed to impair intracellular pH (pH(i)) regulation via vacuolar type H(+)-ATPase in macrophage. We conducted this investigation on Langendorff perfused hearts of rabbits to elucidate the mechanisms involving the NO. precursor L-arginine on myocardial contractile function, glycolysis, mitochondrial respiration, and intracellular alkalinization and tested the effects of amiloride. L-Arginine caused a significant loss of contractile function (96+/-4 mmHg in control, 53+/-16 during L-arginine perfusion, p&lt;0.01) and a significant increase of pH(i) (7.01+/-0.02 prearginine infusion, 7.08+/-0.03 at the end of L-arginine infusion, p&lt;0.01) along with decreased oxygen consumption (MVO(2)) (0.94+/-0.32 ml/min/g dry wt.), increased lactate release, and a loss of creatine phosphate (15% loss). Amiloride could prevent the cell alkalinization and contractile dysfunction, but not the derangement of oxidative metabolism caused by L-arginine in myocytes. We conclude that L-arginine has two distinct effects upon the myocardium: (1) an amiloride-sensitive loss of contractile function associated with intracellular alkalinization; and (2) an amiloride-insensitive inhibition of oxidative metabolism, possibly because of increased myocardial NO. production.

L-Arginine Potentiates Negative Inotropic and Metabolic Effects to Myocardium Partly through the Amiloride Sensitive Mechanism.