Kanagy received a BA in Chemistry from Goshen College (1984) and then worked for Miles Laboratories (Bayer Pharmaceuticals) before going to graduate school at Michigan State University where she received a PhD in Cardiovascular Pharmacology (1992). She completed a Postdoctoral fellowship at the University of Michigan in Cardiovascular Physiology (1995) before joining the department of Cell Biology and Physiology at the University of New Mexico School of Medicine as an Assistant Professor (1995). Kanagy has been part of the Vascular Physiology Group in the Cell Biology and Physiology Department since its formation in 2000.


I have established a productive research laboratory as part of the Vascular Physiology Group at the UNM-HSC. I have also trained 10 PhD students, 6 post-doctoral fellows and numerous undergraduate students. I have an i10 index of 64 and an h-index of 34 with more than 80 publications. I have contributed to the Biomedical Sciences Graduate Program as a mentor, instructor, director and, most recently, as the Senior Associate Dean of Research Education. During my tenure in graduate education leadership we developed several new initiatives including enhanced regional recruitment, expanded professionalism training and additional options for students to prepare for non-academic careers. I also led the Signature Program in Cardiovascular and Metabolic Disease for almost 10 years, instituting an annual Research Symposium and overseeing the pilot grant program to grow the research community in this important area. With over 25 years of experience in cardiovascular research, I have successfully led multiple research projects. My background in vascular physiology includes experience in studying blood pressure regulation, vascular function in animal and human studies, renal function, electrophysiology, live cell calcium imaging, transcriptional regulation and intracellular signaling. Since my appointment as a tenure-track faculty member in 1995, I have been PI or co-Investigator on multiple university-, EPA-, AHA- and NIH-funded grants. I have ongoing collaborations with other members of the Vascular Physiology Group, members of the College of Pharmacy and several physicians including an endocrinologist, a vascular surgeon and a gastroenterologist.


vascular physiology renal physiology cell signaling endothelial cell biology


Distinguished Alumna awardee, Michigan State University (2011) Golden Sovereign award for excellence in Pharmacology Research (2011) Teaching Faculty Award, College of Pharmacy, University of New Mexico (2009) Teacher of the Year Award, School of Medicine, University of New Mexico (2003) Fellow of the Cardiovascular Section of the American Physiological Society (2001 - present) Fellow of the American Heart Association Council for High Blood Pressure Research(1997 - present) NHLBI Hypertension and Microcirculation Study Section (2015 - 2020) American Journal of Heart & Circulatory Physiology, Associate Editor (2008 - 2020) Established Investigator of the American Heart Association (2004-2009)




  • 英语


我的研究集中在心血管生理学的各个方面,主要侧重于外周血管功能的内源性调节剂。 在我的教职生涯早期,研究重点是 α 2 肾上腺素能受体的作用和调节,并提供了一些早期基础工作,将这种受体亚型确立为血管收缩的促成因素,尤其是在患病动脉中。 与 Matthew Campen 教授合作的其他研究调查吸入污染物对血管功能的影响,观察到大鼠吸入相关浓度的柴油废气颗粒后冠状动脉功能受损,这为生活在高浓度地区的个体的冠状动脉事件增加提供了生理基础车辆污染物。 与 Benjimen Walker 教授和 Leif Nelen 教授合作开发了一种睡眠呼吸暂停大鼠模型,以研究睡眠期间长期暴露于缺氧导致血压升高的机制。 我们发现血管收缩肽内皮素的升高导致血压升高。 我的实验室继续确定模拟睡眠呼吸暂停也会通过硫化氢依赖性血管舒张功能受损而损害内皮功能。 从那时起,工作重点是破译这种新型内源性血管舒张剂的血管舒张途径,我们已经发表了几项重要的研究,展示了这种分子如何调节血管功能。 这项工作是当前项目的重点,包括一项临床研究,该研究调查了使用新型透皮传感器评估血管硫化氢产生与已知微血管疾病标志物的相关性。


Graduate Physiology Undergraduate medical student renal physiology


My current work is investigating signaling in the vasculature by the recently described vasodilator, hydrogen sulfide H2S. These studies are some of the first to look at H2S signaling in vascular endothelial cells to cause vasodilation. These studies have identified two animal models with decreased levels of H2S, intermittent hypoxia as a model of sleep apnea and adenine feeding-induced chronic kidney disease. This work is most relevant to the current application and demonstrates my ability to generate and work with animal models and to evaluate H2S signaling. a. Jackson-Weaver O, Paredes DA, Gonzalez Bosc LV, Walker BR, Kanagy NL. Intermittent Hypoxia in Rats Increases Myogenic Tone Through Loss of Hydrogen Sulfide Activation of Large-Conductance Ca2+-Activated Potassium Channels. Circ Res。 2011 10;108(12):1439-47,. PMID 21512160; PMC3234884 b. Naik JS, Osmond JM, Walker BR, Kanagy NL. Hydrogen Sulfide-Induced Vasodilation Mediated by Endothelial TRPV4 Channels. Am J Physiol Heart Circ Physiol。 2016 Dec 1;311(6):H1437-H1444. PMID: 27765747 PMC5206343 c.Gonzalez Bosc LV, Osmond JM, Giermakowska WK, Pace CE, Riggs JL, Jackson-Weaver O, Kanagy NL. NFAT regulation of cystathionine ?-lyase expression in endothelial cells is impaired in rats exposed to intermittent hypoxia. Am J Physiol Heart Circ Physiol。 2017 Apr 1;312(4):H791-H799. PMID: 28130342 PMC5407154. d. Morales-Loredo H, Barrera A, Garcia JM, Pace CE, Naik JS, Gonzalez Bosc LV, Kanagy NL. Hydrogen sulfide regulation of renal and mesenteric blood flow. Am J Physiol Heart Circ Physiol。 2019 Nov 1;317(5):H1157-H1165. PMID: 31625777 PMC6879921 e. Morales-Loredo H, Jones D, Barrera A, Mendiola PJ, Garcia J, Pace C, Murphy M, Kanagy NL, Gonzalez Bosc LV. A dual blocker of endothelin A/B receptors mitigates hypertension but not renal dysfunction in a rat model of chronic kidney disease and sleep apnea. Am J Physiol Renal Physiol. 2019 May 1;316(5):F1041-F1052. PMID 30810064 PMC7132313. Another project has focused on delineating the cardiovascular effects of sleep apnea. 与Dr. Benjimen Walker, we developed an intermittent exposure animal model to investigate the role of elevated endothelin synthesis in the hemodynamic and vascular changes observed with chronic sleep apnea. These studies were some of the first to link endothelin to the hypertension that develops in response to the intermittent hypoxia of sleep apnea. a. Snow J, Kitzis V, Norton C, Torres S, Johnson K, Kanagy NL, Walker BR, and Resta TC. Differential Effects of Chronic and Intermittent Hypoxia on Pulmonary Vasoreactivity. J Applied Physiol 104(1):110-8, 2008. PMID: 17947499; b. Allahdadi KJ, Cherng TW, Pai H, Silva AQ, Walker BR, Nelin LD, Kanagy NL. Endothelin type A receptor antagonist normalizes blood pressure in rats exposed to eucapnic intermittent hypoxia. Am J Physiol Heart Circ Physiol。 2008 Jul;295(1):H434-40. PMID:18515645; PMC2494757 c. Osmond JM, Gonzalez Bosc LV, Walker BR, Kanagy NL. Am J Physiol Heart Circ Physiol。 2014 Mar 1;306(5):H667-73. Endothelin-1-induced vasoconstriction does not require intracellular Ca²? waves in arteries from rats exposed to intermittent hypoxia. PMC3949067 d. Snow JB, Norton CE, Sands MA, Weise-Cross L, Yan S, Herbert LM, Sheak JR, Gonzalez Bosc LV, Walker BR, Kanagy NL, Jernigan NL, Resta TC. Intermittent Hypoxia Augments Pulmonary Vasoconstrictor Reactivity through PKC?/Mitochondrial Oxidant Signaling. Am J呼吸细胞分子生物学。 2020 Jun;62(6):732-746.