With the help of UBRP travel funds I recently traveled to San Diego, California to present my research at the 2008 Experimental Biology Conference. The conference brings together members of the American Physiological Society (APS), the American Society of Biochemistry and Molecular Biology (ASBMB), the American Association of Anatomists (AAA), the American Association of Immunologists (AAI), the American Society for Investigative Pathology (ASIP), the American Society for Nutrition (ASN), and the American Society for Pharmacology and Experimental Therapeutics (ASPET), and boasts an attendance of more than 13,000 scientists, students and industry members.

I was given three opportunities to present my research on the effects of vasopressin on the expression of renal aquaporins and urea transporters in mice with a reduced urinary concentrating ability. As a finalist for the APS's David Bruce Award for Undergraduate Research, I presented my poster to a committee of physiologists from around the country. I also presented in the APS's undergraduate poster session and a more specific poster session on Wednesday that featured posters on research done on the renal concentrating mechanism.

My poster was titled "Long Term Vasopressin Regulation of Renal Aquaporins and Urea Transporters in Mice with a Reduced Urinary Concentration Ability." Aquaporin-1 knockout (AQP1KO) mice have an extremely reduced ability to reabsorb water and also lack an osmotic gradient in their kidneys. In a normal mouse, with an intact osmotic gradient that increases from the cortex to the inner medulla of the kidney, vasopressin up-regulates the expression of aquaporin-2 (AQP2), aquaporin-3 (AQP3) and urea transporter 1 (UTA1) in order to increase water reabsorption in the collecting duct.

In the AQP1KO model, AQP2 and UTA1 mRNA and protein were up-regulated in response to vasopressin. However, in the AQP1KO model there was an up-regulated in AQP3 mRNA but no significant increase in AQP3 protein expression-indicating that the concentration gradient (which is absent in the AQP1KO model) induces some sort of post-transcriptional event that allows for AQP3 to be expressed. This study has significant clinical implications, in particular, for those afflicted diseases characterized by increased levels of circulating vasopressin-such as diabetes and congestive heart failure-who are also being treated for hypertension with loop diuretics-which wash out the concentration gradient.

The weather in San Diego was beautiful, but I was inside most of the time listening to other investigators talk about their research. It was a great opportunity to broaden the depth of my knowledge regarding renal physiology (my field of research) and other, similarly interesting topics, including a talk on how the migratory patterns of blue fin tuna can be used to study climate change.

Overall, attending the conference was a great experience that cemented my intention to pursue a career in research.

Sarah's work is funded in part by a grant from HHMI (52005889).

Sarah Nelson, URBPer in Dr. Heddwen Brooks's lab, Physiology