Meeting Abstract
P3.83 Thursday, Jan. 6 INCREASED EXPOSURE TO RETIONIC ACID ON KIDNEY DEVELOPMENT AND FUNCTION IN THE DEVELOPING CHICKEN Increased Exposure to Retinoic Acid on Kidney Development and Function in the Developing Chicken ALVINE, T.D.*; BURGGREN, W.W.; University of North Texas; University of North Texas travisalvine@my.unt.edu
Developing animals and their organ systems do not operate independently but rather as a group of interactive systems. Blood pressure regulation and fluid homeostasis requires interplay between the heart and kidneys, though the onset of this interaction is poorly understood. Fetal programming results from insults at a critical period that may not become expressed until later in life. Disruption of the normal developmental path of the kidneys, specifically a deficient nephron endowment, has been implicated as a contributing or primary factor in a number of “adult onset” diseases (e.g. kidney disease, and hypertension). Retinoic acid stimulates organogenesis and induces ureteric bud differentiation during kidney development; however overexposure can lead to an inhibitory effect on developing nephrons. To begin to characterize this cross systems interaction, renal modification was induced and renal function was assessed. Eggs of the domestic chicken were given a single injection of retinoic acid on embryonic day 8 of the 21-day incubation period. On days 12, 14, 16, and 18 renal measurements were taken. Using a refined staining technique, identification of actively filtering nephrons was assed in combination with total nephron numbers. Preliminary data indicates that exposure to retinoic acid produced a significant decline in embryo wet mass of 31% during the last days of study. Mass specific kidney and heart masses showed no significant decreases. However, on day 18, a significant decrease in total number of nephrons in treatment (3.44 X 104 ± 5.81 X 103) compared to control (4.34 X 104 ± 7.01 X 103) was seen, but the total number of functional nephrons remained constant. This may be explained by glomerular intermittency whereby nephrons can be recruited when necessary.
