The enzyme nitric oxide synthase plays a role in peripheral vascular disease, a common disease that impairs the mobility of 25 percent of people over the age of 50, according to a Yale study in the Proceedings of the National Academy of Sciences (PNAS).
In a related study this month in the Journal of Clinical Investigation, the same investigator, William Sessa, professor of pharmacology at Yale School of Medicine, found that the protein kinase, Akt1, one of three Akt molecules involved in growth, survival, metabolism and other cellular functions, is responsible for enhancing new blood vessel growth following a blockage due to ischemia.
In the PNAS study Sessa used mice missing the endothelial nitric oxide synthase gene and found they had impaired ability to build arteries and capillaries, which are important for providing blood flow to muscle upon exercise training. Sessa and his colleagues also succeeded in using gene therapy to reverse the effects of the missing gene, which rescued limbs in danger of dying because of ischemia. Ischemia is a severe reduction of blood flow and nutrients, usually because of a blood clot or atherosclerosis.
Sessa said the study in PNAS implies that therapeutic approaches to improve blood flow and arteriogenesis in patients with peripheral vascular disease by using a single cytokine will have limited utility unless impairments in the enzyme nitric oxide function are taken into account and corrected.