PREVENTION OF THE EXCITATORY ACTIONS OF BRADYKININ BY INHIBITION OF PGI(2) FORMATION IN NODOSE NEURONS OF THE GUINEA-PIG

Citation
D. Weinreich et al., PREVENTION OF THE EXCITATORY ACTIONS OF BRADYKININ BY INHIBITION OF PGI(2) FORMATION IN NODOSE NEURONS OF THE GUINEA-PIG, Journal of physiology, 483(3), 1995, pp. 735-746
Citations number
36
Categorie Soggetti
Physiology
Journal title
ISSN journal
00223751
Volume
483
Issue
3
Year of publication
1995
Pages
735 - 746
Database
ISI
SICI code
0022-3751(1995)483:3<735:POTEAO>2.0.ZU;2-B
Abstract
1. Intracellular recordings were made from neurones in intact guinea-p ig nodose ganglia in vitro and from acutely isolated adult guinea-pig and rabbit nodose neurones to study a bradykinin (BK)-mediated block o f a slow spike after-hyperpolarization (AHP(slow)) that is prominent i n 30-40% of these neurones. 2. BK (100 nm) reversibly blocked the AHP( slow), resulting in an ablation of the spike accommodative properties of these neurones. The B1BK receptor agonist [des-Arg(9)]-BK. did not mimic or prevent the actions of BK. In contrast, the B2BK receptor ant agonist D-Arg-[Hyp(3), Thi(5), D-Tic(7), Oic(8)] BK (HOE 140) prevente d BK-induced block of the AHP(slow) and the effect of BK on spike freq uency adaptation. 3. The BK block of the AHP(slow) in acutely dissocia ted neurones was prevented by indomethacin, indicating that this BK ef fect was dependent upon a cyclo-oxygenase metabolite intrinsic to thes e neurones. 4. One to twenty femtomoles of the prostanoids PGE(2), PGD (2), 9 alpha, 11 beta-PGF(2) (a metabolite of PGD(2)), PGF(2 alpha), T xB(2) and PGI(2) were released spontaneously from a nodose ganglion in 15 min. BK (100 nm) selectively increased PGI(2) release 2.8-fold wit hout affecting the release of the other prostanoids. Treatment with 10 mu M tranylcypromine (TCP), a putative PGI(2) synthase inhibitor, com pletely prevented the BK-induced release of PGI(2). 5. In the presence of 10 mu M TCP, BK. no longer produced significant effects on the AHP slow. In contrast, 10 mu M TCP did not prevent PGI(2) from blocking th e AHP(slow). 6. These results suggest that vagal afferents that exhibi t AHP(slow) also possess the B-2 type of BK receptor. Activation of th ese BK receptors results in the production of PGI(2), which in turn co ntrols spike frequency adaptation by affecting the amplitude of the AH P(slow).