Tissue distribution and kininogen gene expression after acute-phase inflammation

Chao, Julie; Swain, Christopher J.; Chao, Steven; Xiong, William; Chao, Lee

doi:10.1016/0304-4165(88)90033-5

Cited by 72 publications

(31 citation statements)

References 13 publications

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“…Although the renal occurrence and localization of tissue kallikrein (Figueroa et al, 1984a(Figueroa et al, ,b,1988Orstavik et al, 1976) and kininogen (Chao et al, 1988;Figueroa et al, 1988;Proud et al, 1981) are well documented, the identification, cellular localization, and subcellular distribution of the kinin B2 receptors in the kidney are unknown. Previous attempts to localize kinin-binding sites in the kidney by ligand autoradiography have focused on microdissected nephron segments from rabbit (Tomita and Pismo.…”

Section: Discussionmentioning

confidence: 99%

Probing for the bradykinin B2 receptor in rat kidney by anti-peptide and anti-ligand antibodies.

Figueroa¹,

González²,

Grigoriev³

et al. 1995

J Histochem Cytochem.

112

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The kallikrein-kinin system is involved in the inflammatory process, in blood pressure regulation, and in renal homeostasis. The presence of kallikreins, kininogens, and kinins in renal tissues and fluids is well established however, the occurrence and distribution of the bradykinin (B2) receptor in the kidney are unknown. Using chemically cross-linked conjugates of bovine serum albumin and the B2 agonist bradykiuin or the potent B2 antagonist HOE140, followed by antibodies to the respective ligand and the peroxidase-anti-peroxidase system, we were able to detect the B2 receptor, The receptor has been found in straight portions of the proximal tubules, in distal straight tubules, in connecting tubules, and in collecting ducts of rat kidney. The staining patterns produced by the ligand conjugate-antiligand approach are in agreement with those obtained by conventional autoradiography using [1251]-Tyro-bradykinin.

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Section: Discussionmentioning

confidence: 99%

Probing for the bradykinin B2 receptor in rat kidney by anti-peptide and anti-ligand antibodies.

Figueroa¹,

González²,

Grigoriev³

et al. 1995

J Histochem Cytochem.

112

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“…The components of the kallikrein-kinin cascade are expressed at distinct sites within the kidney. Kallikrein is localized to cells in the cortical connecting tubule and to a lesser extent in the cortical collecting duct (10,29), and kininogen has been found in the cells of the cortical and medullary collecting ducts (6,12,30). Bradykinin has been shown to be present in interstitial fluid from the cortex and medulla (35,36) and is excreted in urine (2), indicating that it is formed locally in the interstitium and/or in the tubular lumen of the collecting ducts.…”

Section: Discussionmentioning

confidence: 99%

Blockade of renal medullary bradykinin B₂receptors increases tubular sodium reabsorption in rats fed a normal-salt diet

Sivritas

Ploth²,

Fitzgibbon³

2008

American Journal of Physiology-Renal Physiology

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Sivritas S-H, Ploth DW, Fitzgibbon WR. Blockade of renal medullary bradykinin B2 receptors increases tubular sodium reabsorption in rats fed a normal-salt diet. Am J Physiol Renal Physiol 295: F811-F817, 2008. First published July 16, 2008 doi:10.1152/ajprenal.90225.2008.-The present study was performed to test the hypothesis that under normal physiological conditions and/or during augmentation of kinin levels, intrarenal kinins act on medullary bradykinin B2 (BKB2) receptors to acutely increase papillary blood flow (PBF) and therefore Na ϩ excretion. We determined the effect of acute inner medullary interstitial (IMI) BKB2 receptor blockade on renal hemodynamics and excretory function in rats fed either a normal (0.23%)-or a low (0.08%)-NaCl diet. For each NaCl diet, two groups of rats were studied. Baseline renal hemodynamic and excretory function were determined during IMI infusion of 0.9% NaCl into the left kidney. The infusion was then either changed to HOE-140 (100 g ⅐ kg Ϫ1 ⅐ h Ϫ1 , treated group) or maintained with 0.9% NaCl (time control group), and the parameters were again determined. In rats fed a normal-salt diet, HOE-140 infusion decreased left kidney Na ϩ excretion (urinary Na ϩ extraction rate) and fractional Na ϩ excretion by 40 Ϯ 5% and 40 Ϯ 4%, respectively (P Ͻ 0.01), but did not alter glomerular filtration rate, inner medullary blood flow (PBF), or cortical blood flow. In rats fed a low-salt diet, HOE-140 infusion did not alter renal regional hemodynamics or excretory function. We conclude that in rats fed a normal-salt diet, kinins act tonically via medullary BKB2 receptors to increase Na ϩ excretion independent of changes in inner medullary blood flow.inner medullary collecting duct; inner medullary blood flow; renal hemodynamics; renal excretion THE TISSUE KALLIKREIN-KININ-KININASE cascade is a complex enzymatic pathway for the generation of kinin peptides (4). Two of these peptides, bradykinin and lys-bradykinin (kallidin), induce local vasodilation and inhibit renal electrolyte reabsorption by acting as paracrine/autocrine ligands for G proteincoupled bradykinin B 2 (BKB 2 ) receptors (see reviews in Refs. 4 and 18).The kallikrein-kinin systems in brain, kidney, and cardiovascular tissue contribute to the regulation of cardiovascular function and blood pressure (3,5,18,22). However, the renal kallikrein-kinin system (through its action to increase electrolyte and water excretion) plays a primary role in the long-term regulation of blood pressure under conditions of hypertensive insult, especially high salt intake (1,17,19,20,26,41).Paradoxically, although renal kinins are natriuretic, high salt intake suppresses the renal kallikrein-kinin system (28, 44). This suppression is rapid. Cortical and medullary interstitial levels of kinins are markedly reduced within 24 h of exposure to a high-salt diet (36). Conversely, cortical interstitial levels of bradykinin and the activity of the renal kallikrein-kinin system are markedly augmented by low salt intake (28,36,44). This augmentation of t...

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“…In rat cardiac atria and ventricles glandular KLK, its mRNA (2) and low-molecularweight kininogens could be detected (3,4). Coronaries also contain and release KLK (2).…”

Section: The Kallikrein-kinin Systemmentioning

confidence: 99%

Regulation of the kinin receptors after induction of myocardial infarction: a mini-review

Tschöpe

Heringer-Walther

Walther

2000

Braz J Med Biol Res

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It is well known that the responses to vasoactive kinin peptides are mediated through the activation of two receptors termed bradykinin receptor B1 (B1R) and B2 (B2R). The physiologically prominent B2R subtype has certainly been the subject of more intensive efforts in structure-function studies and physiological investigations. However, the B1R activated by a class of kinin metabolites has emerged as an important subject of investigation within the study of the kallikreinkinin system (KKS). Its inducible character under stress and tissue injury is therefore a field of major interest. Although the KKS has been associated with cardiovascular regulation since its discovery at the beginning of the last century, less is known about the B1R and B2R regulation in cardiovascular diseases like hypertension, myocardial infarction (MI) and their complications. This mini-review will summarize our findings on B1R and B2R regulation after induction of MI using a rat model. We will develop the hypothesis that differences in the expression of these receptors may be associated with a dual pathway of the KKS in the complex mechanisms of myocardial remodeling. Key wordsThe kallikrein-kinin system Kinins are biologically active peptides which exert a broad spectrum of physiological effects, including vasodilation, smooth muscle contraction and pain induction. Several kinin peptides have been identified in mammalian species: the nonapeptide bradykinin (BK) and the decapeptide Lys-bradykinin (kallidin) belong to the best investigated members of the kinin family. Kinins are formed by cleavage from precursor kininogens by kallikreins (KLK). They are rapidly degraded by several kininases, including kininase II which is identical to angiotensinconverting enzyme. Kinins exert their effect after stimulation of their cell surface receptors: BK B1 receptor (B1R) and B2 receptor (B2R). Whereas the B2R is responsive to the intact kinins, BK and kallidin, the B1R has a higher affinity for the carboxypeptidase metabolites of kinins, des-Arg 9 -BK and des-

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Tissue distribution and kininogen gene expression after acute-phase inflammation

Cited by 72 publications

References 13 publications

Probing for the bradykinin B2 receptor in rat kidney by anti-peptide and anti-ligand antibodies.

Probing for the bradykinin B2 receptor in rat kidney by anti-peptide and anti-ligand antibodies.

Blockade of renal medullary bradykinin B₂receptors increases tubular sodium reabsorption in rats fed a normal-salt diet

Regulation of the kinin receptors after induction of myocardial infarction: a mini-review

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Tissue distribution and kininogen gene expression after acute-phase inflammation

Cited by 72 publications

References 13 publications

Probing for the bradykinin B2 receptor in rat kidney by anti-peptide and anti-ligand antibodies.

Probing for the bradykinin B2 receptor in rat kidney by anti-peptide and anti-ligand antibodies.

Blockade of renal medullary bradykinin B2receptors increases tubular sodium reabsorption in rats fed a normal-salt diet

Regulation of the kinin receptors after induction of myocardial infarction: a mini-review

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Blockade of renal medullary bradykinin B₂receptors increases tubular sodium reabsorption in rats fed a normal-salt diet