Renal disease profoundly alters cortical interstitial cell function.
Interstitial cells were cultured from explants of the unilaterally hydronephrotic, contralateral, and normal kidneys. Two types of cells were identified in culture, macrophages, and cells which were tentatively identified as fibroblasts. Cells grew at a significantly faster rate in hydronephrotic compared to contralateral or normal kidneys. Cells from the hydronephrotic kidney increased prostaglandin (PG)E2 production in response to bradykinin. Cells from contralateral and normal renal cortex did not increase PGE2 production in response to bradykinin. These results indicate hydronephrosis induces functional changes in interstitial cells cultured from the cortex of hydronephrotic compared to contralateral and normal kidneys. The induction of increased PGE2 synthesis and bradykinin responsiveness in hydronephrotic cortex could be related to the exaggerated prostaglandin synthesis known to occur in hydronephrotic cortex. In hydronephrosis, cortical interstitial cells elaborate increased amounts of substances such as prostaglandins which have the capacity to modulate important parameters of renal function.
D000818:Animals; D001920:Bradykinin / Q000494:pharmacology; D002452:Cell Count; D002478:Cells, Cultured; D000242:Cyclic AMP / Q000378:metabolism; D015232:Dinoprostone; D005347:Fibroblasts / Q000378:metabolism; D006869:Hydronephrosis / Q000378:metabolism / Q000473:pathology*; D007672:Kidney Cortex / Q000378:metabolism / Q000473:pathology*; D008264:Macrophages / Q000378:metabolism; D008297:Male; D011458:Prostaglandins E / Q000378:metabolism; D011817:Rabbits
D011458:Prostaglandins E; D000242:Cyclic AMP; D015232:Dinoprostone; D001920:Bradykinin