Resetting of renal tissular renin-angiotensin and bradykinin-kallikrein systems after unilateral kidney denervation in rats.

Détails

ID Serval
serval:BIB_E1B234760DF6
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Resetting of renal tissular renin-angiotensin and bradykinin-kallikrein systems after unilateral kidney denervation in rats.
Périodique
Histochemistry and cell biology
Auteur⸱e⸱s
Bohlender J.M., Nussberger J., Birkhäuser F., Grouzmann E., Thalmann G.N., Imboden H.
ISSN
1432-119X (Electronic)
ISSN-L
0948-6143
Statut éditorial
Publié
Date de publication
05/2017
Peer-reviewed
Oui
Volume
147
Numéro
5
Pages
585-593
Langue
anglais
Notes
Publication types: Journal Article
Publication Status: ppublish
Résumé
The renal tissular renin-angiotensin and bradykinin-kallikrein systems control kidney function together with the renal sympathetic innervation but their interaction is still unclear. To further elucidate this relationship, we investigated these systems in rats 6 days after left kidney denervation (DNX, n = 8) compared to sham-operated controls (CTR, n = 8). Plasma renin concentration was unchanged in DNX vs. CTR (p = NS). Kidney bradykinin (BK) and angiotensin (Ang) I and II concentrations decreased bilaterally in DNX vs. CTR rats (~20 to 40%, p < 0.05) together with Ang IV and V concentrations that were extremely low (p = NS). Renin, Ang III and dopamine concentrations decreased by ~25 to 50% and norepinephrine concentrations by 99% in DNX kidneys (p < 0.05) but were unaltered in opposite kidneys. Ang II/I and KA were comparable in DNX, contralateral and CTR kidneys. Ang III/II increased in right vs. DNX or CTR kidneys (40-50%, p < 0.05). Ang II was mainly located in tubular epithelium by immunocytological staining and its cellular distribution was unaffected by DNX. Moreover, the angiotensinergic and catecholaminergic innervation of right kidneys was unchanged vs. CTR. We found an important dependency of tissular Ang and BK levels on the renal innervation that may contribute to the resetting of kidney function after DNX. The DNX-induced peptide changes were not readily explained by kidney KA, renin or plasma Ang I generation. However, tissular peptide metabolism and compartmentalization may have played a central role. The mechanisms behind the concentration changes remain unclear and deserve further clarification.
Mots-clé
Angiotensins/metabolism, Animals, Bradykinin/metabolism, Denervation, Kallikreins/metabolism, Kidney/innervation, Kidney/metabolism, Kidney/surgery, Male, Rats, Rats, Wistar, Renin/metabolism, Angiotensin, Bradykinin, Kidney, Sympathetic
Pubmed
Web of science
Création de la notice
28/02/2017 19:52
Dernière modification de la notice
25/06/2022 6:34
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