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Abstract
Nitric oxide (NO), a gaseous transmitter in the noradrenergic–noncholinergic nervous system and a paracrine agent formed in the vascular endothelial cells from the amino acid L-arginine, mediates vasodilatory commands from the endothelium to the smooth muscle cells. In the tissues responsible for aqueous formation and its outflow all components necessary for NO formation have been found. Therefore, its physiological role in the regulation of intraocular pressure is more than plausible. Numerous preclinical but a limited number of clinical studies support the possibility of using NO-releasing compounds to treat elevated intraocular pressure; for example, in glaucoma. Despite a quarter-century of lasting research interest in this field, no real breakthrough has been reached. Problems in local kinetics and local adverse effects have lowered the interest, and more clinical evidence is needed to verify this attractive theory.
Financial & competing interests disclosure
The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
No writing assistance was utilized in the production of this manuscript.