Abstract

Sodium nitroprusside (NP) was found to decrease the tissue lactate level under conditions of high (HiOxSa) and low (hypoxia) oxygen saturation in spontaneously beating rat atria. Nitroprusside also increased the level of cyclic GMP (cGMP) in a dose-dependent manner in both states. The time course and dose dependence of these effects suggest that cGMP might be responsible for the decreased tissue level of lactate demonstrated. The findings suggest that cGMP might inhibit lactate production in HiOxSa and antagonize the hypoxia-induced acceleration of anaerobic metabolism. It is proposed that a state of low-rate glycolysis results from this inhibitory effect of cGMP. Furthermore, the possible role of cGMP as a feed-back regulator of the redox state is discussed in the light of these findings.

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