Key result
Preincubation with exogenous GTP significantly enhanced sodium nitrite-induced relaxation of rat mesenteric arteries (58% vs 34%) and inhibition of ADP-induced platelet aggregation.
Why the study?
Does exogenous GTP enhance the effects of sodium nitrite on vascular smooth muscle relaxation and platelet aggregation in rat mesenteric arteries and human platelets?
Does exogenous GTP enhance the effects of sodium nitrite on vascular smooth muscle relaxation and platelet aggregation in rat mesenteric arteries and human platelets?
Absolute Event Rate: 58% vs 34%
Exogenous GTP enhances sodium nitrite-induced stimulation of guanylate cyclase, leading to increased vascular smooth muscle relaxation and inhibition of platelet aggregation in preclinical models.
GTP-nitrite interactions are hypothesis-generating in vitro; clinical relevance and translation require further study.
Exogenous guanosine triphosphate (GTP) (1-2 x 10(-4)M) resulted in increased concentrations of cyclic GMP both in endothelium denuded rat mesenteric artery (RMA) and in human ADP-stimulated platelets. Sodium nitrite (3.3 x 10(-4)M) relaxed precontracted RMA by 34%. When the arteries were preincubated with GTP (2 x 10(-4)M) sodium nitrite administration resulted in a significantly greater relaxation (58%) of the RMA with concomitant 2-fold increase in cGMP. Sodium nitrite (1 x 10(-4)M) had an inhibitory effect on ADP-induced platelet aggregation. Preincubation with GTP enhanced significantly the sodium nitrite-induced inhibition of ADP-induced platelet aggregation with a simultaneous 5-fold increase in cGMP. These results indicate that exogenous GTP enhances the sodium nitrite-induced stimulation of guanylate cyclase and thus enhances the effects of sodium nitrite on arterial smooth muscle and platelets.
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Laustiola et al. (1991) studied this question. Exogenous GTP and Sodium nitrite vs. Sodium nitrite alone was evaluated on Vascular smooth muscle relaxation. Preincubation with exogenous GTP significantly enhanced sodium nitrite-induced relaxation of rat mesenteric arteries (58% vs 34%) and inhibition of ADP-induced platelet aggregation.
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