31st Annual Student Research Conference
Renal Lymphatic Alterations In Angiotensin II-Induced Hypertension
Micaela E. Saathoff
Dr. Brett M. Mitchell (Texas A&M University College of Medicine) and Ms. Anne Bergey, Faculty Mentors
Hypertension is a pervasive health concern affecting one in three American adults, and is associated with renal immune cell infiltration and inflammation. De novo renal lymphatic vessel (RLV) formation, exhibited in cases of human renal allografts and kidney disease, is triggered by inflammation. Therefore, RLV formation is considered a compensatory mechanism to drain immune cells and excess interstitial fluid from sites of renal injury. We hypothesized that RLVs would increase in number during angiotensin II-induced hypertension, corroborated by gene expression changes of markers for immune cells, kidney injury, and RLV formation. Upon data analysis using RT-qPCR, immunofluorescence, and blood pressure readings, our results indicated that angiotensin-II caused hypertension, renal immune cell infiltration, and kidney injury; however, for unknown reasons, RLV density was not increased. In summary, angiotensin II caused HTN, renal immune cell infiltration, and kidney injury. The effects of angiotensin II on RLVs will be determined in future studies.
Keywords: hypertension, renal lymphatic vessel formation, angiotensin II, inflammation, lymphatic system
Topic(s):Biology
Presentation Type: Poster
Session: 3-6
Location: GEO - SUB
Time: 3:30