Among its direct effects, the stimulation of pro-inflammatory enzymes in the vasculature [e.g., thromboxane synthase, cyclooxygenase-1 (COX-1), and COX-2] and reactive oxygen species generation in vascular smooth muscle cells may decrease nitric oxide (NO) bioavailability and lead to increased vasoconstriction, increased blood pressure, and renal dysfunction [48]. Here, PTGS1 is linked to Abnormal renal physiology.