Differential induction of functional B1-bradykinin receptors along the rat nephron in endotoxin induced inflammation

Marin‐Castaño, Maria E.; Schanstra, Joost P.; Praddaude, Françoise; Pesquero, João Bosco; Ader, J. L.; Girolami, Jean Pierre; Bascands, Jean-Loup

doi:10.1046/j.1523-1755.1998.00201.x

Cited by 33 publications

(33 citation statements)

References 46 publications

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“…Controls ( Figure 4B and D) for contaminating genomic DNA amplification and relative quantification with GAPDH were performed as described previously. 19 As eval- uated by this method, high B 1 -receptor mRNA expression was observed in the efferent arteriole, glomeruli, medullary thin descending limb, inner medullary thin limb, and distal tubule; moderate expression was found in the proximal convoluted tubule, proximal straight tubule, medullary thick ascending limb, and cortical collecting duct; and low expression was observed in the outer medullary collecting duct after ACE inhibition. As previously reported, 19 expression of B 2 -receptor mRNA was observed in all nephron segments of control rats, and ACE inhibition was without significant effect in B 2 -receptor mRNA in the different nephron segments (data not shown).…”

Section: Chronic Ace Inhibition Induces B 1 -Receptor Mrna Expressionmentioning

confidence: 74%

“…19 The following nephron segments were isolated: glomeruli, efferent arteriole, proximal convoluted tubule, proximal straight tubule, medullary thin descending limb, inner medullary thin limb, medullary thick ascending limb, distal tubule, and cortical and outer medullary collecting ducts. Glomerular and tubular surfaces were measured as described previously.…”

Section: Microdissection Of Rat Nephron Segmentsmentioning

confidence: 99%

“…Semiquantitative B 1 -and B 2 -receptor and GAPDH mRNA expression in microdissected nephron segments (1 glomerulus, surface 480Ϯ80 m 2 , or a total surface of 480Ϯ89 m 2 of each renal tubule segment) was analyzed and semiquantified by reverse transcription-polymerase chain reaction (RT-PCR) followed by Southern blot analysis as described previously. 19 …”

Section: Mrna Expression Analysismentioning

confidence: 99%

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Induction of Functional Bradykinin B ₁ -Receptors in Normotensive Rats and Mice Under Chronic Angiotensin-Converting Enzyme Inhibitor Treatment

et al. 2002

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Background-The physiological effects of ACE inhibitors may act in part through a kinin-dependent mechanism. We investigated the effect of chronic ACE-inhibitor treatment on functional kinin B 1 -and B 2 -receptor expression, which are the molecular entities responsible for the biological effects of kinins. Methods and Results-Rats were subjected to different 6-week treatments using various mixtures of the following agents:ACE inhibitor, angiotensin AT 1 -receptor antagonist, and B 1 -and B 2 -receptor antagonists. Chronic ACE inhibition induced both renal and vascular B 1 -receptor expression, whereas B 2 -receptor expression was not modified. Furthermore, with B 1 -receptor antagonists, it was shown that B 1 -receptor induction was involved in the hypotensive effect of ACE inhibition. Using microdissection, we prepared 10 different nephron segments and found ACE-inhibitor-induced expression of functional B 1 -receptors in all segments. ACE-inhibitor-induced B 1 -receptor induction involved homologous upregulation, because it was prevented by B 1 -receptor antagonist treatment. Finally, using B 2 -receptor knockout mice, we showed that ACE-inhibitor-induced B 1 -receptor expression was B 2 -receptor independent. Conclusions-This study provides the first evidence that chronic ACE-inhibitor administration is associated with functional vascular and renal B 1 -receptor induction, which is involved in ACE-inhibitor-induced hypotension. The observed B 1 -receptor induction in the kidney might participate in the known renoprotective effects of ACE inhibition.

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Section: Chronic Ace Inhibition Induces B 1 -Receptor Mrna Expressionmentioning

confidence: 74%

Section: Microdissection Of Rat Nephron Segmentsmentioning

confidence: 99%

Section: Mrna Expression Analysismentioning

confidence: 99%

See 1 more Smart Citation

Induction of Functional Bradykinin B ₁ -Receptors in Normotensive Rats and Mice Under Chronic Angiotensin-Converting Enzyme Inhibitor Treatment

et al. 2002

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“…3,4 Under experimental renal inflammation, a marked upregulation of the B1R expression along the rat nephron has been reported. 5,6 In this inflammatory context, it has been shown that the B1R agonist is able to upregulate the expression of its own receptor via the activation of transcription factor NF-B. 7,8 The activated B1R stimulates the release of proinflammatory cytokines including TNF-␣ and IL-1 9 and is also involved in leukocyte accumulation and activation.…”

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confidence: 99%

Blockade of the Kinin B1 Receptor Ameloriates Glomerulonephritis

Klein¹,

Gonzalez²,

Decramer³

et al. 2010

Journal of the American Society of Nephrology

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Severe inflammation characterizes rapidly progressive glomerulonephritides, and expression of the kinin B1 receptor (B1R) associates with inflammation. Delayed B1R blockade reduces renal inflammation in a model of unilateral ureteral obstruction, but whether B1R modulates the pathophysiology of glomerulonephritides is unknown. Here, we observed an association of B1R protein expression and inflammation, in both glomeruli and the renal interstitium, in biopsies of patients with glomerulonephritides, HenochSchö nlein purpura nephropathy, and ANCA-associated vasculitis. In the nephrotoxic serum-induced glomerulonephritis model, we observed upregulation of the B1R receptor; treatment with a B1R antagonist beginning 2 weeks after the onset of disease reduced both glomerular and tubular lesions and improved renal function. B1R blockade reduced renal chemokine expression and macrophage accumulation. Collectively, our data demonstrate that blockade of the kinin B1R has significant potential for the treatment of glomerulonephritis. Rapidly progressive glomerulonephritides constitute a group of kidney diseases sharing common pathologic features. These nephropathies are characterized by severe glomerular inflammation, mainly composed of infiltrating macrophages and T cells. This leads to the formation of glomerular crescents composed of immune and proliferating epithelial cells from the Bowman's capsule. After the primary glomerular insult, inflammation and lesions extend to the tubulointerstitial compartment and induce tubular damage and progressive interstitial fibrosis, leading to the loss of renal function; therefore, renal inflammation is a key player in the initiation and the progression of these pathologies. It has been suggested that any strategy or agent able to limit or attenuate renal inflammation should significantly slow the progression of glomerulonephritides to ESRD. 1 Endogenous kinins (bradykinin-related peptides)are produced through cleavage of kininogens by kallikreins. These peptides mediate their biologic effects by activation of two G protein-coupled receptors: a constitutively expressed B2 receptor (B2R) and an inducible B1 receptor (B1R). 2 Bradykinin and kallidin are the natural agonists of the B2R, whereas their metabolites, generated by the enzyme kininase I, desArg9-BK and Lys-des-Arg9-BK, respectively, are spe-

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“…The B1R is now widely recognized as an inducible receptor, and its expression is up-regulated following injuries such as myocardial infarction (21), balloon-induced injury of the carotid artery (22), and LPS injection in the rat kidney (23). Up-regulation of B1R also occurs under the control of specific cytokines released under conditions of trauma or stress, including interleukin-1β and tumor necrosis factor-α (24,25).…”

Section: Discussionmentioning

confidence: 99%

Renal Protective Role of Bradykinin B1 Receptor in Stroke-Prone Spontaneously Hypertensive Rats

et al. 2004

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The kallikrein-kinin system plays important roles in blood pressure regulation, metabolism of electrolytes and organ protection. Although the bradykinin B2 receptor (B2R) has been reported to be involved in most of these effects, a role of the bradykinin B1 receptor (B1R) has also been noted recently. The aim of this study was to determine the role of renal B1R in stroke-prone spontaneously hypertensive rats (SHR-SP). Sixteen

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Differential induction of functional B1-bradykinin receptors along the rat nephron in endotoxin induced inflammation

Abstract: These studies show a functional induction of the B1-kinin receptor along the rat nephron, which should be taken in account to address the effects of kinins under inflammatory conditions in the kidney.

Cited by 33 publications

References 46 publications

Induction of Functional Bradykinin B ₁ -Receptors in Normotensive Rats and Mice Under Chronic Angiotensin-Converting Enzyme Inhibitor Treatment

Induction of Functional Bradykinin B ₁ -Receptors in Normotensive Rats and Mice Under Chronic Angiotensin-Converting Enzyme Inhibitor Treatment

Blockade of the Kinin B1 Receptor Ameloriates Glomerulonephritis

Renal Protective Role of Bradykinin B1 Receptor in Stroke-Prone Spontaneously Hypertensive Rats

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Differential induction of functional B1-bradykinin receptors along the rat nephron in endotoxin induced inflammation

Abstract: These studies show a functional induction of the B1-kinin receptor along the rat nephron, which should be taken in account to address the effects of kinins under inflammatory conditions in the kidney.

Cited by 33 publications

References 46 publications

Induction of Functional Bradykinin B 1 -Receptors in Normotensive Rats and Mice Under Chronic Angiotensin-Converting Enzyme Inhibitor Treatment

Induction of Functional Bradykinin B 1 -Receptors in Normotensive Rats and Mice Under Chronic Angiotensin-Converting Enzyme Inhibitor Treatment

Blockade of the Kinin B1 Receptor Ameloriates Glomerulonephritis

Renal Protective Role of Bradykinin B1 Receptor in Stroke-Prone Spontaneously Hypertensive Rats

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Induction of Functional Bradykinin B ₁ -Receptors in Normotensive Rats and Mice Under Chronic Angiotensin-Converting Enzyme Inhibitor Treatment

Induction of Functional Bradykinin B ₁ -Receptors in Normotensive Rats and Mice Under Chronic Angiotensin-Converting Enzyme Inhibitor Treatment