Intrarenal angiotensin and bradykinin peptide levels in the remnant kidneymodel of renal insufficiency

Citation
Fe. Mackie et al., Intrarenal angiotensin and bradykinin peptide levels in the remnant kidneymodel of renal insufficiency, KIDNEY INT, 59(4), 2001, pp. 1458-1465
Citations number
37
Categorie Soggetti
Urology & Nephrology","da verificare
Journal title
KIDNEY INTERNATIONAL
ISSN journal
00852538 → ACNP
Volume
59
Issue
4
Year of publication
2001
Pages
1458 - 1465
Database
ISI
SICI code
0085-2538(200104)59:4<1458:IAABPL>2.0.ZU;2-M
Abstract
Background. The remnant kidney model of renal failure is associated with no rmal or suppressed plasma renin and angiotensin (Ang) II levels when hypert ension is established. However? the hypertension responds to angiotensin-co nverting enzyme (ACE) inhibition and Ang II receptor antagonism, suggesting a role for Ang II in the hypertensive process. Bradykinin (BK) is a potent vasoactive peptide that may also participate in this model. Methods. Ang IL and BK peptides were measured in the ischemic peri-infarct portion and the intact portion of the remnant kidney at two, five, and seve n weeks after surgery. Plasma Ang II, renin, angiotensinogen, and aldostero ne levels were also measured. Results. Ang II levels in the peri-infarct portion were higher than in the intact portion at ail time points and were higher than in sham-operated kid ney at two weeks. Ang II levels in the intact portion were similar to the l evels in kidneys of sham-operated rats at two and five weeks and were suppr essed at seven weeks. BK levels were increased in the peri-infarct portion at all time points and in the intact portion at two and five weeks. Plasma Ang II and aldosterone levels were also elevated at two weeks. Conclusions Peri-infarct renal tissue Ang II levels and plasma Ang TT and a ldosterone levels increase transiently during the evolution of hypertension in the remnant kidney model. Sustained hypertension is associated with an increase in intrarenal BK levels but not with persistent increases in intra renal or circulating Ang II levels.