Premium
Prostaglandin E2 inhibits and indomethacin enhances noradrenaline release in isolated kidneys of adult spontaneously hypertensive rats.
Author(s) -
Rump LC,
Wilde K.,
Schollmeyer P.
Publication year - 1990
Publication title -
british journal of clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.216
H-Index - 146
eISSN - 1365-2125
pISSN - 0306-5251
DOI - 10.1111/j.1365-2125.1990.tb05495.x
Subject(s) - endocrinology , medicine , prostaglandin e2 , kidney , stimulation , inhibitory postsynaptic potential , prostaglandin , chemistry , norepinephrine , receptor , prostaglandin e , neurotransmission , dopamine
Renal neurotransmission and its modulation by prostaglandin (PG) E2 (0.06 microM) and indomethacin (10 microM) was investigated in isolated kidneys of adult spontaneously hypertensive (SHR) and normotensive control (WKY) rats. After preincubation with [3H]‐noradrenaline the renal nerves were stimulated. The stimulation induced (S‐I) outflow of radioactivity was taken as an index of noradrenaline release. The S‐I outflow of radioactivity from SHR and WKY kidneys was similar but S‐I pressor responses were enhanced in kidneys of SHR. PGE2 inhibited and indomethacin enhanced the S‐I outflow of radioactivity in kidneys of WKY and SHR to a similar extent. This inhibitory effect of PGE2 is due to activation of inhibitory prejunctional PGE2 receptors. Neuronally released noradrenaline stimulates a local formation of PGE2 which then transjunctionally inhibits noradrenaline release. Renal noradrenaline release in the adult SHR and its modulation by PGs is not altered. An enhanced postjunctional responsiveness of the renal vasculature may contribute to the maintenance of hypertension in the adult SHR.