Prostaglandins, a link between renal hydro- and hemodynamic in dogs.
An increase of the intrarenal pressure to 40 mmHg induced by ureteral constriction or by kidney compression is shown to be followed by increased renal blood flow in anesthetized dogs. This hyperemia is probably the result of enhanced  intrarenal prostaglandin activity since it is followed by increased urinary prostaglandin E excretion and is abolished by indomethacin pretreatment. The increase of renal blood flow seems to be due to dilation of the afferent arteriole in order to maintain the filtration pressure. The glomerular filtration rate is thus severely depressed in indomethacin pretreated dogs. Urine and electrolyte excretion is comparably redcued during elevated intrarenal pressure in non-pretreated and in indomethacin pretreated dogs, which suggests that factors other than glomerular filtration rate are involved. Urine osmolarity is positively correlated with renal blood flow, and urine osmolarity increases during elevated intrarenal pressure in non pretreated dogs, whilst urine osmolarity remains unchanged in dogs pretreated with indomethacin.
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002712:Chlorides / Q000652:urine; D004285:Dogs; D005260:Female; D005919:Glomerular Filtration Rate / Q000187:drug effects; D007213:Indomethacin / Q000494:pharmacology; D007668:Kidney / Q000098:blood supply / Q000502:physiology*; D009994:Osmolar Concentration; D011188:Potassium / Q000652:urine; D011312:Pressure; D011458:Prostaglandins E / Q000378:metabolism / Q000652:urine; D012039:Regional Blood Flow / Q000187:drug effects; D012964:Sodium / Q000652:urine; D014556:Urine
D002712:Chlorides; D011458:Prostaglandins E; D012964:Sodium; D011188:Potassium; D007213:Indomethacin