Prostaglandins and Renin Release The Effect of PGI2, PGE2, and 13,14-Dihydro PGE2 on the Baroreceptor Mechanism of Renin Release in the Dog

We compared the ability of the vasodilator prostaglandins PGE2, PGE2, and 13,14-dlhydro PGE2 to release renin when infused into the denervated, nonfiltering canine kidney in vivo. Papaverine was used as a nonprostaglandin vasodilator. All the prostaglandins tested were capable of stimulating renin s...

Full description

Saved in:
Bibliographic Details
Published in:Circulation research 1979-06, Vol.44 (6), p.796-799
Main Authors: GERBER, JOHN G, KELLER, ROBERT T, NIES, ALAN S
Format: Article
Language:English
Subjects:
Animals
Blood Pressure - drug effects
Denervation
Dogs
Epoprostenol - pharmacology
Female
Indomethacin - pharmacology
Kidney - blood supply
Kidney - innervation
Kidney - metabolism
Male
Pressoreceptors - drug effects
Propranolol - pharmacology
Prostaglandins E, Synthetic - pharmacology
Prostaglandins, Synthetic - pharmacology
Renin - blood
Renin - metabolism
Citations: Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:We compared the ability of the vasodilator prostaglandins PGE2, PGE2, and 13,14-dlhydro PGE2 to release renin when infused into the denervated, nonfiltering canine kidney in vivo. Papaverine was used as a nonprostaglandin vasodilator. All the prostaglandins tested were capable of stimulating renin secretion, with the scale of potency being 13,14-dihydro PGE2 > PGI2 > PGE2; papaverine had no effect on renin secretion. These results indicate that both PGE2 and PGI2 can stimulate renin secretion but that vasodilation per se is not a stimulus. 13,14-Dihydro PGE2 was included because it is a poorer substrate than PGE2, both for transport into cells and catabolism to inactive products, but has comparable potency to PGE2 when tested in systems with limited ability to catabolize PGE2. The fact that 13,14-dihydro PGE2 was the most potent prostaglandin tested suggests that the effects ofPGE2 in our system are reduced by the kidneysʼ recognized ability to extract and catabolize PGE2. Since PGIfis less avidly metabolized than PGE2 by the kidney, the differences in observed potency between PGE2 and PGE2 could be largely the result of differences in renal catabolism of the two prostaglandins rather than differences in intrinsic potency. Therefore, both PGE2 and PGI2 are candidates for the endogenous prostaglandin responsible for stimulating renin secretion. Circ Res 44796-799, 1979
ISSN:0009-7330
1524-4571
DOI:10.1161/01.res.44.6.796