Release of PGE and PGI2 in the pump-perfused dog kidney and associated hypotension.
The mechanism of enhanced renal prostaglandin (PG) release in the in situ pump-perfused kidney was studied in anesthetized dogs. Pump perfusion caused a gradual decrease in mean arterial blood pressure (BP) from 163 to 128 mmHg over an 80-min period. The renal arteriovenous level of PGE and plasma renin activity (PRA) were increased by a mean of 1.36 ng/ml and 22 ng AI.ml-1.h-1, respectively. In a second group of dogs treated with captopril, pump perfusion did not alter PGE or BP, but increased PRA. When the animals were treated with indomethacin, the renal arteriovenous levels of PGE and 6-keto-PGF1 alpha were not changed but PRA increased during the 80 min of pump perfusion. In a fourth group of dogs that had undergone renal denervation and phentolamine treatment, changes in PGE and BP occurred during pump perfusion similar to the changes in the control group, and 6-keto-PGF1 alpha release by the kidney also increased. The results indicate that renal PG release during group perfusion is mainly due to the activation of the renin-angiotensin system and that the hypotension due to pump perfusion is PG mediated.
D015121:6-Ketoprostaglandin F1 alpha; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002216:Captopril / Q000494:pharmacology; D004285:Dogs; D011464:Epoprostenol / Q000378:metabolism*; D005260:Female; D007022:Hypotension / Q000503:physiopathology*; D007213:Indomethacin / Q000494:pharmacology; D007668:Kidney / Q000187:drug effects / Q000378:metabolism*; D007700:Kinetics; D008297:Male; D011453:Prostaglandins / Q000378:metabolism*; D011458:Prostaglandins E / Q000378:metabolism*; D011460:Prostaglandins F / Q000378:metabolism; D012083:Renin / Q000097:blood
D011453:Prostaglandins; D011458:Prostaglandins E; D011460:Prostaglandins F; D015121:6-Ketoprostaglandin F1 alpha; D002216:Captopril; D011464:Epoprostenol; D012083:Renin; D007213:Indomethacin