Research Alert

Newswise — Research published ahead of print in the journal Function identifies the molecular pathways through which nitric oxide promotes dilation of the blood vessels. Nitric oxide is a compound produced by the endothelial cells that line the blood vessels. The compound relaxes smooth muscle cells and plays an important role in heart health.

“In this study, we show that [nitric oxide (NO)] causes vasodilation by inhibiting the activity of Ca2+-dependent TRPM4 (transient receptor potential melastatin 4) cation channels. Probing further, we found that NO does not act directly on TRPM4 but instead initiates a signaling cascade that inhibits its activation by blocking the release of Ca2+ from the sarcoplasmic reticulum. Thus, our findings reveal the essential molecular pathways of NO-induced vasodilation—a fundamental unresolved concept in cardiovascular physiology,” the researchers wrote.

Read the full article, “Nitric oxide signals through IRAG to inhibit TRPM4 channels and dilate cerebral arteries.” Contact APS Media Relations to schedule an interview with the research team.

Journal Link: Function