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The effects of prostaglandin E2 (PGE)2 and the thromboxane A2 (TxA2) receptor agonist U-46619 on noradrenaline release and pressor responses to renal nerve stimulation (RNS) at 1 Hz were investigated in isolated kidneys of spontaneously hypertensive rats (SHR; 5–7 weeks) and age-matched Wistar–Kyoto rats (WKY). After incubation with 3H-noradrenaline, the renal nerves were stimulated. The stimulation-induced (S-l) outflow of radioactivity was taken as an index of noradrenaline release. Absolute S-l outflow of radioactivity was lower in SHR than in WKY but pressor responses to RNS were greater in SHR than in WKY. Tetrodotoxin (1 µmol/l) abolished S-l outflow of radioactivity and pressor responses to RNS in both strains. PGE2 (0.06 µmol/l) inhibited S-l outflow of radioactivity in SHR but not in WKY kidneys. PGE2 (0.6 µmol/l) inhibited S-l outflow of radioactivity in both strains. In SHR, PGE2 (0.6 µmol/l) decreased pressor responses to RNS, but increased them in WKY. In WKY, but not in SHR kidneys, pressor responses to RNS were markedly reduced by the ɑ1-adrenoceptor antagonist prazosin (0.1 µmol/l). The prazosin-resistant pressor responses to RNS were blocked by ɑ,ß-methylene adenosine triphosphate (ATP; 1 µmol/l). In kidneys of SHR, pretreated with 6-OH-dopamine (50 mg/kg intravenously, 24 and 48h before isolation of the kidneys) to destroy sympathetic nerve endings, pressor responses to RNS and S-l outflow of radioactivity were almost abolished. U-46619 (0.1 µmol/l) increased perfusion pressure in SHR and WKY kidneys and this effect was blocked by the TxA2 receptor antagonist daltroban (BM 13505; 3µmol/I). U-46619 did not significantly modulate S-l outflow of radioactivity. The results suggest that activation of prejunctional PGE2 receptors in kidneys of SHR and WKY inhibits noradrenaline release. The prejunctional inhibitory PGE2 receptor mechanism on renal sympathetic nerves seems to operate more effectively in SHR than in WKY. There is no evidence for prejunctional TxA2 receptors in the kidneys of SHR or WKY. Pressor responses to RNS at 1 Hz in SHR kidneys seem to be due entirely to release of a purinergic co-transmitter from renal sympathetic nerves, and PGE2 possibly reduces pressor responses to RNS by inhibiting release of this purinergic co-transmitter.