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

• Published in: Histochemistry and cell biology Vol. 147; no. 5; pp. 585 - 593
• Main Authors: Bohlender, Jürgen M., Nussberger, Jürg, Birkhäuser, Frédéric, Grouzmann, Eric, Thalmann, George N., Imboden, Hans
• Format: Journal Article
• Language: English
• Published: Berlin/Heidelberg Springer Berlin Heidelberg 01.05.2017; Springer Nature B.V
• Subjects: Angiotensins - metabolism; Animals; Biochemistry; Biomedical and Life Sciences; Biomedicine; Bradykinin - metabolism; Cell Biology; Cellular biology; Denervation; Developmental Biology; Kallikreins - metabolism; Kidney - innervation; Kidney - metabolism; Kidney - surgery; Kidneys; Male; Original Paper; Rats; Rats, Wistar; Renin - metabolism; Rodents; Tissues; Bradykinin; Kidney; Sympathetic; Angiotensin; Denervation
• ISSN: 0948-6143; 1432-119X
• DOI: 10.1007/s00418-017-1543-y

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.