ArticleAmerican journal of physiology. Renal physiology2008
Blockade of renal medullary bradykinin B2 receptors increases tubular sodium reabsorption in rats fed a normal-salt diet.
Article in American journal of physiology. Renal physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 22 citations in OpenAlex.
- Effects of intrarenal afferent stimulation by bradykinin on renal sympathetic nerve activity: tonic inhibition contributing to renal function.Pflugers Archiv : European journal of physiology · 2025Article
- Kinins and chymase: the forgotten components of the renin-angiotensin system and their implications in COVID-19 disease.American journal of physiology. Lung cellular and molecular physiology · 2021Review
- Chronic Overexpression of Bradykinin in Kidney Causes Polyuria and Cardiac Hypertrophy.Frontiers in medicine · 2018Article
- Imbalance in Renal Vasoactive Enzymes Induced by Mild Hypoxia: Angiotensin-Converting Enzyme Increases While Neutral Endopeptidase Decreases.Frontiers in physiology · 2018Article
- Direct regulation of ENaC by bradykinin in the distal nephron. Implications for renal sodium handling.Current opinion in nephrology and hypertension · 2014Review
- Salt-dependent inhibition of epithelial Na+ channel-mediated sodium reabsorption in the aldosterone-sensitive distal nephron by bradykinin.Hypertension (Dallas, Tex. : 1979) · 2012Article
- Loss of renal medullary endothelin B receptor function during salt deprivation is regulated by angiotensin II.American journal of physiology. Renal physiology · 2012Article
- Bradykinin acutely inhibits activity of the epithelial Na+ channel in mammalian aldosterone-sensitive distal nephron.American journal of physiology. Renal physiology · 2011Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
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 B(2) (BKB(2)) receptors to acutely increase papillary blood flow (PBF) and therefore Na(+) excretion. We determined the effect of acute inner medullary interstitial (IMI) BKB(2) 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 microg.kg(-1).h(-1), 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(+) excretion (urinary Na(+) extraction rate) and fractional Na(+) excretion by 40 +/- 5% and 40 +/- 4%, respectively (P < 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 BKB(2) receptors to increase Na(+) excretion independent of changes in inner medullary blood flow.
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Registered trials
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