ARGINASE &NO SYNTHASE &ACTIVITY IN SKIN: EFFECTS OF ESSENTIAL HYPERTENS &AGE

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Hypertensive vascular disease (HT) is characterized by alterations in neurotransmitter signals leading to impaired dilation of blood vessels in skin and other organs. HT causes changes in nitric oxide (NO) availability that lead to reduced vasodilation of blood vessels. In the skin, NO is a key signaling molecule involved in vascular tone and responses to thermal stimuli. HT can decrease NO production by 1) increased arginase activity and 2) decreased NO-synthase activity. Changes in arginase and NO-synthase activity in human skin have not been explored. We propose to examine arginase and NO-synthase activity in skin punch biopsies using Western blot analysis and immunohistochemistry.