New York Medical College

Wenhui Wang, M.D.

Professor of Pharmacology

Dr. WangEmail:


Department of Pharmacology
Basic Sciences Building
New York Medical College
Valhalla, NY 10595

Professional Interests:

My laboratory is focused on studying the regulation of Na+ and K+ transport in aldosterone-sensitive distal tubules of the kidney. Na+ is a major extracellular ion and plays a key role in maintaining extracellular volum, and decreasing extracellular Na+ content can result in hypotension whereas increasing Na+ content causes hypertension. Conversely, K+ is mainly located in the intracellular fluid and extracellular K+ must be maintained in a narrow range: either high plasma K+ (hyperkalemia) or low plasma K+ (hypokalemia) can cause life-threatening cardiac arrhythmias. The kidney plays a key role in secreting K+ to match the dietary K+ intake, and disorders of K+ balance are common in patients with kidney failure.

We have two research projects funded by the National Institutes of Health.

Regulation and Modulation of Renal K+ channels in Kidney
Molecular, biochemical and electrophysiological approaches are being used to study the molecular mechanisms involved in the reguation of renal K+ channels. We have found that protein tyrosine kinases and WNK+ (with-no-lysine kinase) play an important role in the regulation of renal K+ secretion. Using miRNA+ array we have also identified several miRNA+ that regulate renal K+ channels - these include miR-802, miR-192 and miR142-3P.

Regulation of Epithelial Na+ Channels by epoxyeicosatrienoic acids (EETs)
Arachidonic acid can be metabolized to EETs by the cytochrome P450 epoxygenase CYP2C44, and we have found that EETs play an important role in the regulation of Na+ transport in the distal nephron. High Na+ intake stimulates CYP2C44 activity and thus inhibits Na+ absorption in the distal nephron, and defective regulation of CYP2C44 can cause the salt-sensitive hypertension. We are currently using genetically modified mice to study the role of CYP2C44 in regulating epithelial Na+ channels in the kidney.

Education Profile:

Post Graduate Studies  

Graduate Degree:   M.D.

Graduate Degree Institution:   University of Innsbruck (Austria)

Undergraduate Institution:  

Selected Bibliography:

Dimin Li, Zhijian Wang, Peng Sun, Yan Jin, Dao-Hong Lin, Steven C. Hebert, Gerhard Giebisch and Wen-Hui Wang. Inhibition of MAPK+ stimulates the Ca2+-dependent big-conductance K+ channels in cortical collecting duct. PNAS 103;19569-19574, 2006.

Yuan Wei, Beth Zavilowitz, Lisa M. Satlin, and Wen-Hui Wang. Angiotensin II Inhibits the ROMK-like Small Conductance K+ Channel in Renal Cortical Collecting Duct during Dietary Potassium Restriction, J.Bio.Chem, 282:6455-6462, 2006.

Peng Sun, Wen Liu, Dao-Hong Lin, Peng Yue, RoweNa+ Kemp, Lisa M. Satlin, and Wen-Hui Wang. Epoxyeicosatrienoic Acid Activates BK+ Channels in the Cortical Collecting Duct, J Am Soc Nephrol 20: 513–523, 2009.

Peng Yue, Dao-Hong Lin, Chun-Yang Pan, Qiang Leng, Gerhard Giebisch, Richard P. Lifton, and Wen-Hui Wang, Src family protein tyrosine kinase (PTK) modulates the effect of SGK1 and WNK4 on ROMK+ channels. PNAS . 106: 15061–15066, 2009.

Dao-Hong Lin, Peng Yue, Chu-Yang Pan, Peng Sun, Xin Zhang, Zeguang Han, Marcel Roos, Michael Caplan, Gerhard Giebisch, and Wen-Hui Wang. POSH Stimulates the Ubiquitination and the Clathrin-independent Endocytosis of ROMK1 Channels. J. Biol. Chem. 284: 29614–29624, 2009.

Chen, Y-J, Li, Jing and Quilley, J. Deficient renal 20-HETE release in the diabetic rat is not the result of oxidative stress. Am. J. Physiol. 294:H2305-H2312, 2008.