Key result
Low-dose (1-10 nM) nitroglycerin triggers constitutive endothelial nitric oxide synthase (NOS) activation, which is a fundamental requirement for its vasorelaxation action in wild-type animals.
Nitroglycerin-induced vasorelaxation at pharmacologically relevant concentrations fundamentally requires endothelial NOS activation.
Supports eNOS requirement for nitroglycerin vasorelaxation in animals; leaves open translation to clinical settings.
The physiological effects of nitroglycerin as a potent vasodilator have long been documented. However, the molecular mechanisms by which nitroglycerin exerts its biological functions are still a matter of intense debate. Enzymatic pathways converting nitroglycerin to vasoactive compounds have been identified, but none of them seems to fully account for the reported clinical observations. Here, we demonstrate that nitroglycerin triggers constitutive nitric oxide synthase (NOS) activation, which is a major source of NO responsible for low-dose (1-10 nM) nitroglycerin-induced vasorelaxation. Our studies in cell cultures, isolated vessels, and whole animals identified endothelial NOS activation as a fundamental requirement for nitroglycerin action at pharmacologically relevant concentrations in WT animals.
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Bonini et al. (2008) studied this question. Nitroglycerin was evaluated on Endothelial NOS activation and vasorelaxation. Low-dose (1-10 nM) nitroglycerin triggers constitutive endothelial nitric oxide synthase (NOS) activation, which is a fundamental requirement for its vasorelaxation action in wild-type animals.
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