L-Arginine hydrochloride serve as substrates and nitrogen donors for endothelial nitric oxide synthase (eNOS) to produce nitric oxide (NO). They are transported into vascular smooth muscle cells via cationic amino acid transporters, where they are metabolized into NO, polyamines, or L-proline. As effective vasodilators, they are commonly used to induce experimental acute pancreatitis models.

In individuals with sickle cell anemia, oral administration of L-Arginine (0.1 g/kg) significantly reduces pulmonary arterial systolic pressure after 5 days. Continuous treatment with L-Arginine (4 mg/kg per minute for 1 hour) in rabbit limbs subjected to regional ischemia/reperfusion reduced superoxide production by cNOS, thereby increasing NO accumulation. In SV-129 mice, subcutaneous injection of L-Arginine (2 mg/kg) resulted in the upregulation of eNOS.

Treatment with L-Arginine (0.3 mM) for 30 minutes significantly increases nitric oxide (NO) production in bovine aortic endothelial cells exposed to n-LDL and oxidized-LDL.