Dr. Li is an Associate Professor at the George Washington University Medical Center and is an attending physician at the Washington DC Veterans Affairs Medical Center. He has a deep interest in the field of hypertension from a basic science and clinical perspective. After graduating from medical school he completed an extensive research fellowship in pharmacology at Wake Forest University which propelled him into the arena of hypertension. He is a recipient of a Young Investigator Award for “Non-peptide AT1 Receptor Antagonist Losartan Inhibits Thromboxane A2 Induced Platelet Aggregation and Vascular Contractions in Spontaneously Hypertensive Rats” supported by the Council for High Blood Pressure Research of the American Heart Association. Dr. Li then pursued further research in hypertension at Georgetown University and eventually completed a fellowship in nephrology there. He actively works on hypertension research and clinics through the Hypertension Center at the Washington DC VA Medical Center in conjunction with cardiology.
Training:
- Research Fellowship: Wake Forest University (Pharmacology)
- Internship: Albert Einstein College of Medicine 2001 (Internal Medicine)
- Residency: at Seton Hall University in 2003 (Internal Medicine)
- Fellowship: Georgetown University Hospital 2008 (Nephrology)
Clinical Service:
- Nephrology and hypertension
- Internal medicine
Expertise:
- Clinical nephrology and hypertension
- Public health and clinical epidemiology
Research
Dr. Li's early research focused on the regulation of vascular tone, blood pressure, kidney blood flow by angiotensin peptides, nitric oxide, carbon monoxide and estrogen. Currently he is interested in the sympathetic regulation of blood pressure in chronic kidney disease and renal denervations in resistant hypertension.
Community Service
Member of local American Society of Hypertension, and American Chinese Physician Association, Atlantic chapter.
- Brosnihan KB, Li P, Figueroa J, Ganten D, Ferrario CM. Estrogen, nitric oxide and hypertension differentially modulate agonist-induced contractile responses in female transgenic (mRen2)27 hypertensive rats. Am J Physiol Heart Circ Physiol. 294; H-1995-H2001, 2008
- Li, P, Houli Jiang, LiMing Yang, Shuo Quan, Sandra Dinocca, Francise Rodriguez, Nader G. Abraham, and Alberto Nasjletti. Angiotensin II Induces Ccarbon Monoxide Production in the Perfused Kidney: Relation to Protein Kinase C Activation. Am J physiol (Renal physiol) 10.1152, 2004
- Li P, Fukuhara M, DI Diz, Ferrario CM and Brosnihan KB. Novel AT1 receptor antagonist Irbesartan prevents thromboxane A2-induced vasoconstriction in canine coronary arteries and human platelet aggregation. Journal of Pharmacology and Experimental Therapeutics. 290(1): 149-54, 2000.
- Li P, Ferrario CM, and Brosnihan KB. Losartan blocks thromboxane A2 induced platelet aggregation and vascular contractions in spontaneously hypertensive rats. Journal of cardiovascular pharmacology, 32: 198-205, 1998.
- Li P, Ferrario CM, Ganten D, Brosnihan KB. Chronic estrogen treatment in female transgenic (mRen2) 27 hypertensive rats augments endothelium-derived nitric oxide release. American Journal of Hypertension. 10:662-670, 1997.
- Li P, Chappell MC, Ferrario CM, Brosnihan KB. Angiotensin (1-7) augments bradykinin-induced vasodilation by competing with ACE and releasing nitric oxide. Hypertension. 29 (part 2): 394-400. 1997
- Li P, Ferrario CM, Brosnihan KB. Non-peptide angiotensin II antagonist Losartan inhibits thromboxane A2 induced contractions in canine coronary arteries. Journal of Pharmacology and Experimental Therapeutics. 281:1065-1070, 1997
- Brosnihan, KB, Li P, Ferrario CM. Angiotensin-(1-7) dilates canine coronary arteries through kinins and nitric oxide. Hypertension. 27 (part 2): 523-528. 1996.
- Li P, Tong C, Eisenach JC, and Figueroa JP. NMDA causes release of nitric oxide from rat spinal cord in vitro. Brain Research. 637:287-291, 1994.