Research shows nitric oxide mediates anti-inflammatory effects in specific conditions, highlighting the significance of nitroglycerin's vasodilatory action.
In 1987, it was demonstrated that nitric oxide (NO) is the endothelium-derived relaxing factor (EDRF). This opened a long history of confirming that NO is synthesized in all tissues through constitutive synthases in the endothelium and nervous system, and inducible synthases in cells of the immune system. In parallel, it was proven that nitrovasodilators (NVDs), such as Glyceryl Trinitrate (GTN), are transformed into NO and develop their vasodilatory action through the action of the NO/cGMP pathway. In 1990, we verified that transdermic GTN, in addition to relaxing smooth muscle cells, also had anti-inflammatory effects in inflammatory processes accessible via this route, such as Superficial Thrombophlebitis or Supraspinatus Tendonitis. Ten years later, other authors began to confirm this effect of transdermal GTN, confirming the primacy of our publications in the description of this action.
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J. A. Fernández (2025) studied this question.
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