Nitric oxide (NO) is a signaling molecule produced by three isoforms of nitric oxide synthase (NOS): neuronal NOS (nNOS), inducible NOS (iNOS), and endothelial NOS (eNOS). All NOS isoforms use L-arginine and oxygen, along with cofactors such as NADPH, FAD, FMN, and BH4, to generate NO. NOS proteins are homodimers that bind calmodulin and contain a heme group. nNOS is expressed in neurons and plays roles in synaptic plasticity, blood pressure regulation, and penile erection. iNOS is induced by inflammatory signals and produces large amounts of NO, contributing to inflammation and septic shock. eNOS is primarily found in endothelial cells and helps maintain vascular tone, prevent atherosclerosis, and control blood pressure. However, oxidative stress, eNOS uncoupling, and endothelial dysfunction can impair these functions. Pharmacological agents such as renin-angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and statins can reduce oxidative stress and restore eNOS function. NO also plays roles in various physiological processes, including vasodilation, platelet inhibition, and angiogenesis. In pathophysiology, excessive NO production can lead to oxidative stress, endothelial dysfunction, and atherosclerosis. Drugs that interfere with the renin-angiotensin-aldosterone system and statins have pleiotropic effects that improve endothelial function and reduce cardiovascular risk. Understanding the regulation and function of NOS isoforms is crucial for developing therapeutic strategies targeting NO-related diseases.Nitric oxide (NO) is a signaling molecule produced by three isoforms of nitric oxide synthase (NOS): neuronal NOS (nNOS), inducible NOS (iNOS), and endothelial NOS (eNOS). All NOS isoforms use L-arginine and oxygen, along with cofactors such as NADPH, FAD, FMN, and BH4, to generate NO. NOS proteins are homodimers that bind calmodulin and contain a heme group. nNOS is expressed in neurons and plays roles in synaptic plasticity, blood pressure regulation, and penile erection. iNOS is induced by inflammatory signals and produces large amounts of NO, contributing to inflammation and septic shock. eNOS is primarily found in endothelial cells and helps maintain vascular tone, prevent atherosclerosis, and control blood pressure. However, oxidative stress, eNOS uncoupling, and endothelial dysfunction can impair these functions. Pharmacological agents such as renin-angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and statins can reduce oxidative stress and restore eNOS function. NO also plays roles in various physiological processes, including vasodilation, platelet inhibition, and angiogenesis. In pathophysiology, excessive NO production can lead to oxidative stress, endothelial dysfunction, and atherosclerosis. Drugs that interfere with the renin-angiotensin-aldosterone system and statins have pleiotropic effects that improve endothelial function and reduce cardiovascular risk. Understanding the regulation and function of NOS isoforms is crucial for developing therapeutic strategies targeting NO-related diseases.