Submitted on November 14, 2007
Accepted on July 11, 2008
Mechanisms of neonatal increase in glomerular filtration rate
Anita J Turner1, Russell D Brown2, Mattias Carlstrom3, Karen Jane Gibson1*, and A. Erik G. Persson2
1 Dept of Physiology, School of Medical Sciences, University of New South Wales, Sydney, New South Wales, Australia
2 Dept of Physiology, School of Medical Sciences, University of New South Wales, Sydney, New South Wales, Australia; Dept of Medical Cell Biology, Division of Integrative Physiology, University of Uppsala, Sweden
3 Dept of Medical Cell Biology, Division of Integrative Physiology, University of Uppsala, Sweden
* To whom correspondence should be addressed. E-mail: k.gibson{at}unsw.edu.au.
To investigate the mechanisms responsible for the neonatal increase in glomerular filtration rate (GFR), renal function studies (whole kidney and micropuncture) were carried out in anesthesized fetal sheep (133-140 days gestation; term = 150 days) and lambs (12-18 days). Fetuses were delivered and placed in a water bath (39.5°C), keeping the umbilical cord moist and intact. Lambs were studied on a thermostatically controlled heating pad. Animals were prepared for either blood flow studies or micropuncture measurements. Expected differences in blood composition, cardiovascular and renal function were observed between fetuses and lambs, and values obtained for most variables were similar to those measured in chronically catheterized unanesthetized animals. Fetal GFR was much lower than that of lambs (0.20 vs 0.62 ml min-1 g kidney-1, P<0.001). Free-flow, stop-flow and net filtration pressures (NFP) were lower in the fetuses than the lambs (NFP 20.8 vs 23.8 mmHg, P<0.001) as was the calculated ultrafiltration coefficient (0.014 vs 0.022 ml min-1 g-1 mmHg-1, P<0.001). Thus it is concluded that rises in both net filtration pressure and the ultrafiltration coefficient contribute to the large increase in GFR between fetal life and ~ 2 weeks after birth.
