Localization of components of the kallikrein-kinin system in the kidney: relation to renal function. State of the art lecture.

Vio, Carlos P.; Loyola, Steev; Velarde, Victoria

doi:10.1161/01.hyp.19.2_suppl.ii10

Cited by 35 publications

(27 citation statements)

References 39 publications

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“…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. Kinin binding sites have been localized on renal tubular cells, most notably collecting tubules (21,37,42,43) and interstitial cells (14,46). Furthermore, the BKB 2 receptors have been localized to both the luminal and basolateral membranes of proximal and distal straight tubules, cortical connecting tubules, and cortical and medullary collecting ducts (11,43).…”

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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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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“…The kallikrein-kinin system is a vasoactive system that seems to participate in complex events such as regulation of blood pressure, control of the extracellular volume, sodium and water excretion, renal vascular resistance, and renin release. 16,17 We have previously demonstrated that urinary kallikrein is increased in normal rat pregnancy. 9,11 In the rat, the highest kallikrein levels are observed at midpregnancy, attaining prepregnancy values toward term.…”

Section: Salas Et Al Water Deprivation In Pregnant Rats 337mentioning

confidence: 97%

Renal and Hormonal Effects of Water Deprivation in Late-Term Pregnant Rats

Salas

Giacaman²,

Vío³

2004

Hypertension

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Abstract-Water-retaining hormones are stimulated during pregnancy allowing normal volume expansion. Because pregnant rats actively retain water, we postulate that water deprivation (WD) would cause a greater reduction in plasma volume in pregnant than in nonpregnant rats. To test this hypothesis, Sprague-Dawley pregnant and nonpregnant rats were water-deprived for 48 hours. At day 19 of pregnancy, or in the corresponding day in nonpregnant rats, they were randomly assigned to either a WD or a control (C) pair-fed group (nϭ10 to 12 per group). WD significantly reduced body weight, food intake, and creatinine clearance, and increased urinary osmolality in nonpregnant and pregnant rats. WD reduced plasma volume in a similar proportion in nonpregnant and pregnant rats (nonpregnant rats Cϭ13.1Ϯ0.

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“…1 " 3 Intravenous administration of an inhibitor of neutral endopeptidase, the major kininase in the rat kidney, 4 selectively increased renal inner medullary (papillary) blood flow in anesthetized rats. 3 This effect was blocked by a kinin receptor antagonist, indicating that an elevation of endogenous kinins can alter medullary blood flow. Similar results have been demonstrated during angiotensin converting enzyme inhibition.…”

Section: Orphological and Functional Data Indicate Thatmentioning

confidence: 99%

Kinin actions on renal papillary blood flow and sodium excretion.

Mattson

Cowley

1993

Hypertension

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Infusion of bradykinin into the renal medullary interstitium (0.1 /ig/min, n=6) significantly increased renal papillary blood flow as measured by laser-Doppler flowmetry to 117±3% of control without altering cortical blood flow or blood pressure in anesthetized Munich-Wistar rats. In animals prepared for clearance studies, renal medullary bradykinin infusion did not alter total renal blood flow, glomerular filtration rate, or renal interstitial hydrostatic pressure but increased urine flow by 100%, sodium excretion by 111%, and fractional sodium excretion by 107%. No changes occurred in mean arterial pressure or contralateral kidney function during the interstitial bradykinin infusion. Blockade of endogenous kinin degradation by interstitial infusion of captopril (1 mg/hr) significantly increased papillary blood flow by 21 ±5% without altering cortical blood flow. Pretreatment with the nitric oxide inhibitor jV c -nltro-L-arginine-methyI ester (2 fig/mia, n=l) eliminated the increase in papillary blood flow associated with either bradykinin or captopril infusion. We conclude that renal medullary interstitial infusion of bradykinin increases sodium and water excretion, which is associated with a selective increase in papillary blood flow by a nitric oxide-dependent mechanism. kinins may act as paracrine agents in the renal medulla. 1 " 3 Intravenous administration of an inhibitor of neutral endopeptidase, the major kininase in the rat kidney, 4 selectively increased renal inner medullary (papillary) blood flow in anesthetized rats.3 This effect was blocked by a kinin receptor antagonist, indicating that an elevation of endogenous kinins can alter medullary blood flow. Similar results have been demonstrated during angiotensin converting enzyme inhibition. Although cortical blood flow increases during inhibition of converting enzyme because of decreased angiotensin II levels, renal medullary blood flow increases because of increased kinins. 6 ' 7 These data indicate that kinins have a primary influence on the renal medullary circulation in the rat. In support of these functional data, morphological data indicate that the intrarenal site of kinin formation and release is in the distal connecting tubule and collecting duct. 1 -3 It is therefore thought that the peptide exerts its physiological effects from the luminal or the interstitial side of the collecting duct in the renal medulla. Previous studies examining the renal hemodynamic and excretory effects of exogenous bradykinin were performed by renal arterial infusion. "10 This route of infusion may not mimic a physiological route of kinin delivery, because intrarenally formed kinins must reach the vasculature via the interstitium. To address this problem, we have recently developed an infusion technique in our laboratory by which compounds can be infused and localized in the renal medullary interstitium. 1112The purpose of the present study was to characterize the effects of renal medullary interstitial infusion of bradykinin on the intrarenal distribution o...

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Localization of components of the kallikrein-kinin system in the kidney: relation to renal function. State of the art lecture.

Cited by 35 publications

References 39 publications

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

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

Renal and Hormonal Effects of Water Deprivation in Late-Term Pregnant Rats

Kinin actions on renal papillary blood flow and sodium excretion.

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Localization of components of the kallikrein-kinin system in the kidney: relation to renal function. State of the art lecture.

Cited by 35 publications

References 39 publications

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

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

Renal and Hormonal Effects of Water Deprivation in Late-Term Pregnant Rats

Kinin actions on renal papillary blood flow and sodium excretion.

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Resources

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

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