Influence of bradykinin B1 and B2 receptors in the immune response triggered by renal ischemia–reperfusion injury

Wang, Pamella Huey Mei; Cenedeze, Marcos Antônio; Pesquero, João Bosco; Pacheco-Silva, Álvaro; Câmara, Niels Olsen Saraiva

doi:10.1016/j.intimp.2006.07.031

Cited by 18 publications

(15 citation statements)

References 47 publications

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“…In contrast to the consensus that ACEIs have beneficial effects on I/R injury, previous reports are conflicting with respect to the effects of pharmacological agents interacting with the bradykinin receptors (20)(21)(22). In addition, several studies have suggested that agonism of the B1R and B2R may have different effects on the severity of I/R injury (21)(22)(23).…”

Section: Discussionmentioning

confidence: 97%

“…In addition, several studies have suggested that agonism of the B1R and B2R may have different effects on the severity of I/R injury (21)(22)(23). In contrast, lack of the B1R (42) or B2R (43) aggravates the I/R injury in the heart and brain of mice, whereas adenovirus-mediated gene transfer of tissue kallikrein protects against ischemic stroke in rats (44).…”

Section: Discussionmentioning

confidence: 99%

“…In contrast to the consensus that ACEIs have beneficial effects on I/R injury, previous studies have produced conflicting results concerning the effect on I/R injury in different organs of stimulating the two bradykinin receptors, B1R and B2R (20)(21)(22). In addition, several studies have suggested that agonism of the B1R may have opposite effects from agonism of the B2R on the severity of I/R injury (23).…”

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confidence: 98%

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Bradykinin B1 and B2 receptors both have protective roles in renal ischemia/reperfusion injury

Kakoki

McGarrah

Kim

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

120

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To explore the role of the kallikrein-kinin system in relation to ischemia/reperfusion injury in the kidney, we generated mice lacking both the bradykinin B1 and B2 receptor genes (B1RB2R-null, Bdkrb1 ؊/ ؊/Bdkrb2 ؊/؊ ) by deleting the genomic region encoding the two receptors. In 4-month-old mice, blood pressures were not significantly different among B1RB2R-null, B2R-null (Bdkrb2 ؊/؊ ), and WT mice. After 30 min of bilateral renal artery occlusion and 24 h of reperfusion, mortality rates, renal histological and functional changes, 8-hydroxy-2 -deoxyguanosine levels in total DNA, mtDNA deletions, and the number of TUNEL-positive cells in the kidneys increased progressively in the following order (from lowest to highest): WT, B2R-null, and B1RB2R-null mice. Increases in mRNA levels of TGF-␤1, connective tissue growth factor, and endothelin-1 after ischemia/reperfusion injury were also exaggerated in the same order (from lowest to highest): WT, B2R-null, and B1RB2R-null. Thus, both the B1 and B2 bradykinin receptors play an important role in reducing DNA damage, apoptosis, morphological and functional kidney changes, and mortality during renal ischemia/reperfusion injury.hypoxia ͉ mitochondria ͉ oxidative stress I schemic tissue injuries, including stroke, myocardial infarction, and ischemic acute renal failure, are devastating complications in patients with hypertension, diabetes, atherosclerosis, and senescence. In organ transplantation, damage to allografts during any ischemic period before the transplant markedly influences short-term and long-term graft function and outcome (1). Furthermore, although reoxygenation after ischemia is essential for cell survival, damage also develops during the reperfusion period. Previous studies have shown that acute ATP depletion, intracellular Ca 2ϩ accumulation, and increased generation of reactive oxygen species by mitochondria all play important roles in the pathogenesis of ischemia/reperfusion (I/R) injury (2).Angiotensin-I-converting enzyme (ACE) inhibitors (ACEIs) reduce not only chronic cardiovascular remodeling after ischemia but also acute tissue injury caused by I/R in the heart (3), lung (4), liver (5), and kidneys (6, 7). Several observations indicate that the beneficial effects of ACEIs in the acute phase are mainly due to activation of the bradykinin nitric oxide (NO) cascade as a result of inhibition of the inactivation of bradykinin, rather than due to suppression of angiotensin II formation. Thus, ACEIs are much more effective than angiotensin type I receptor antagonists in protecting against I/R (8-10), and bradykinin B2 receptor (B2R) antagonists and NO synthase blockers markedly attenuate the protective effects of ACEIs (8, 9, 11).Bradykinin and lysyl-bradykinin (kallidin) are generated from kininogens by the kallikreins and some other serine proteases. ACE, which is a carboxydipeptidase, inactivates both peptides by removing two amino acids from their carboxyl termini. In mammals, at least two receptors have been identified: the bradykinin B1 receptor (B...

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Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 98%

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Bradykinin B1 and B2 receptors both have protective roles in renal ischemia/reperfusion injury

Kakoki

McGarrah

Kim

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

120

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“…In our study, HO-1 was also higher in B1KO. Previously, we observed that in an acute model of renal injury B1KO protection was associated with augmented HO-1 expression [35]. Both obstructed and non-obstructed kidneys presented high levels of HO-1.…”

Section: Discussionmentioning

confidence: 76%

“…Besides that, it can also modulate the secretion of prostaglandins [28], mastocytes mediators [29], cytokines [30,31], chemokines and leukotrienes from different types of cell [32][33][34]. Moreover, in an acute model of renal insult B1R deletion exerted cytoprotective effects by immune downregulation [35]. Considering these, we believe that the B1R may modify inflammatory responses found in UUO.…”

Section: Discussionmentioning

confidence: 99%