Effects of growth hormone and IGF-I on glomerular ultrafiltration in growth hormone-deficient rats

In growth hormone deficient states glomerular filtration rate (GFR) and renal plasma flow rate (RPF) are both reduced. Studies were performed in growth hormone deficient rats to delineate the physiologic mechanisms by which growth hormone and IGF-I contribute to the regulation of glomerular function. Growth hormone deficient dw/dw rats received, for one week, subcutaneous infusions of vehicle, des(1-3)IGF-I or were injected i.m. with recombinant human growth hormone. Subsequent renal micropuncture and clearance studies revealed a low GFR and single nephron GFR (SNGFR) in vehicle treated growth hormone deficient animals. Glomerular function became normal with growth hormone or IGF-I treatment, respectively. Both treatments raised SNGFR by reducing arteriolar resistance and increasing the glomerular ultrafiltration coefficient. Furthermore, the two treatments also increased the glomerular tuft volume and the kidney weight which may contribute to the rise in SNGFR and GFR. It is concluded that, (1) in growth hormone deficiency glomerular function is reduced secondary to a high renal arteriolar resistance and a low ultrafiltration coefficient. Both result from a lack in IGF-I rather than the growth hormone deficiency state per se. (2) The growth hormone-IGF-I axis may contribute to the maintenance and physiologic regulation of GFR.