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

精氨酸酶

• 批准号: 7625850
• 负责人: LACY HOLOWATZ
• 金额: $ 0.11万
• 依托单位: PENNSYLVANIA STATE UNIV HERSHEY MED CTR
• 依托单位国家: 美国
• 财政年份: 2007
• 资助国家: 美国
• 起止时间: 2007-04-01 至 2008-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7625850
• 关键词: Age; Blood Vessels; Computer Retrieval of Information on Scientific Projects Database; Funding; Grant; Human; Hypertension; Immunohistochemistry; Institution; Lead; Neurotransmitters; Nitric Oxide; Nitric Oxide Synthase; Organ; Production; Punch Biopsy; Research; Research Personnel; Resources; Signal Transduction; Signaling Molecule; Skin; Source; Stimulus; United States National Institutes of Health; Vasodilation; Western Blotting; arginase; response

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.

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 高血压血管疾病（HT）的特征是神经递质信号的改变，导致皮肤和其他器官的血管扩张受损。 HT引起一氧化氮（NO）可用性的变化，导致血管舒张减少。 在皮肤中，NO是参与血管张力和对热刺激的反应的关键信号分子。 HT可通过1）增加过氧化物酶活性和2）降低NO合酶活性来降低NO的产生。 人类皮肤中的过氧化物酶和一氧化氮合酶活性的变化还没有被探索过。 我们建议使用蛋白质印迹分析和免疫组织化学检查皮肤穿刺活检中的过氧化物酶和NO合酶活性。