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University of Washington
School of Medicine
Box 358050
850 Republican Street
Brotman Building 453
Seattle, WA 98195-8050

Kanchan Chitaly, PhD


Dr. Kanchan Chitaley

Dr. Chitaley received her PhD from the Department of Physiology at the University of Michigan under the guidance of the internationally known hypertension expert, Dr. Clinton Webb. her post-doctoral training was conducted at the Department of Surgery at the University of Washington under the mentorship of the Dr. Alexander Clowes. Through basic science, epidemiological and clinical research, members of her laboratory aim to elucidate the mechanism(s) of vascular disease. This includes general vascular inflammation associated with chronic air pollution exposure, as well as penile vascular disease and the resultant erectile dysfunction associated with diabetes. The lab's ultimate goal is to identify potential new therapeutic avenues to restore vascular health. Their approach includes the use of a wide range of molecular, physiologic and epidemiological tools. Examples of some active research projects:

General Vascular Disease

Vascular Reactivity Following Chronic Air Pollution Exposure

Center Grant NIH (PI: Kauffman; Project 3 PI: Chitaley)
Air pollution exposures are associated with cardiovascular disease, especially atherosclerotic disease such as myocardial infarction. Increasing evidence indicates that the major source of variation in air pollution's cardiovascular health effects is from exposure to traffic. The studies in our recently funded DISCOVER Center involve human, basic animal and epidemiologic evaluation. Specifically, our project (Project 3 of the Center) is in collaboration with Francis Kim (University of Washington) and Stephan VanEeeden (University of British Columbia) and involves examining mechanisms that underlie systemic and vascular inflammation following diesel exhaust exposure in mice.

ED Related

The role of elastin in veno-occlusive function and type II diabetic-ED

R01 NIH (PI: Chitaley)
The outer layer of the corpus cavernosum, the tunica albuginea, is rich in elastic fibers and has the capacity to expand in response to the force of blood pressure, resulting in an increased length and diameter of the penis. However, the expandability of the tunica is finite, and ultimately the initial rise in intracavernosal pressure (ICP) along with the opposing force of the tunica albuginea activates a mechanical occlusion or “sandwiching” of the venous outflow. Thus, the combined inflow of blood following penile arteriole and sinusoidal dilation, as well as subsequent veno-occlusion, result in maintained elevation of ICP and erection. We recently found that db/db mice, a common mouse model of type II diabetes, have a veno-occlusive disorder that stems from a lack of tissue filling due, in part, to altered vasoreactivity consistent with impaired cavernosal relaxant ability. We also showed that these mice have may impairment in tissue distensability resulting from altered deposition of fibrillar collagen and elastin. Elastic fibers are assembled extracellularly and are comprised of elastin and specific microfibrillar proteins. In this project, we hypothesize that elastin deposition and fiber formation is critical for proper erectile function and that this process is altered in type II diabetic mice, resulting in impaired veno-occlusive function and erectile dysfunction. As elastin degradation is also known to occur in tissue following smoking and/or aging, this knowledge gained from this proposal may also have implications for erectile dysfunction associated with these risk factors as well.