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.

Personal Statement

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.

Areas of Specialty

vascular physiology
renal physiology
cell signaling
endothelial cell biology


BA in Chemistry from Goshen College (1984)

PhD in Cardiovascular Pharmacology from Michigan State University (1992)

Postdoctoral fellowship at the University of Michigan in Cardiovascular Physiology (1995)

Achievements & Awards

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)




  • English


My research has focused on various aspects of cardiovascular physiology with primary emphasis on endogenous regulators of peripheral vascular function. Studies early in my faculty career focused on the role and regulation of alpha 2 adrenergic receptors and provided some of the early groundwork establishing this receptor subtype as contributors to vasoconstriction, especially in diseased arteries.  Other studies in collaboration with Professor Matthew Campen investigating the impact of inhaled pollutants on vascular function observed impairment of coronary artery function in rats after inhalation of relevant concentrations of diesel exhaust particles providing a physiological basis for elevated coronary events in individuals living in areas with high levels of vehicle pollutants.  Collaborations with Professors Benjimen Walker and Leif Nelen developed a rat model of sleep apnea to study the mechanisms leading to increased blood pressure with chronic exposure to hypoxia during sleep.  We found that elevations in the vasoconstrictor peptide, endothelin, contributed to the increased blood pressure. My laboratory went on to determine that simulated sleep apnea also impairs endothelial function through impairments in hydrogen sulfide dependent vasodilation. Work since then has focused on deciphering the vasodilatory pathway of this novel endogenous vasodilator and we have published several important studies showing how this molecule regulates vascular function. This work is the focus of current projects including a clinical study investigating the use of a novel transdermal sensor to evaluate the correlation of vascular hydrogen sulfide production with known markers of microvascular disease.

Courses Taught

Graduate Physiology
Undergraduate medical student renal physiology

Research and Scholarship

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. In collaboration with 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 Respir Cell Mol Biol. 2020 Jun;62(6):732-746. PMID: 32048876