Literature DB >> 2140836

A regulatory role for large vessels in organ circulation. Endothelial cells of the main renal artery modulate intrarenal hemodynamics in the rat.

V Kon1, R C Harris, I Ichikawa.   

Abstract

After arterial denudation by external rubbing of the left main renal artery, we assessed renal plasma flow rate (RPF) and glomerular filtration rate (GFR) in left and right kidneys of Munich-Wistar rats before and after intravenous infusion of acetylcholine (ACH), atrial natriuretic peptide (ANP), or nitroprusside (NP). In the right kidney RPF and/or GFR increased in response to both endothelium-derived relaxing factor (EDRF)-dependent (i.e., ACH) and -independent vasodilators (i.e., ANP and NP); on average, RPF rose by 22 +/- 4% (P less than 0.005), 19 +/- 10% (P less than 0.005), and 37 +/- 12% (P greater than 0.05), respectively. By contrast, in the left kidney RPF failed to increase after ACH (falling by 23 +/- 10%, P less than 0.001) and rose only in response to ANP and NP. To further evaluate the main renal artery's contribution to renal vasodilation, ACH and another EDRF-dependent agent, histamine, were infused through a micropipette into either the proximal or distal portions of the endothelium-intact renal artery. Proximal infusion of ACH led to increases in RPF and GFR, on average by 8 +/- 2% (P less than 0.025) and 10 +/- 3% (P less than 0.01), while bypassing the arterial endothelium by distal infusion failed to increase RPF and GFR, which fell by 24 +/- 6% (P less than 0.025) and 22 +/- 6% (P less than 0.005), respectively. Similarly, proximal infusion of histamine increased RPF by 12 +/- 3% (P less than 0.05), while distal infusion was virtually without effects on plasma flow. Micropuncture study during intravenous ACH infusion revealed significantly higher afferent and efferent arteriolar resistances and lower ultrafiltration coefficients in denuded versus nondenuded kidneys. These data indicate that the main renal artery is a major regulator of renal blood flow and vascular resistances. Similar to other endothelium-derived substances, EDRF may be elaborated mainly by large vessels and may act on the downstream microcirculatory systems, which determine organ blood flow and transcapillary fluid transfer.

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Year:  1990        PMID: 2140836      PMCID: PMC296633          DOI: 10.1172/JCI114628

Source DB:  PubMed          Journal:  J Clin Invest        ISSN: 0021-9738            Impact factor:   14.808


  26 in total

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  8 in total

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Authors:  E Tchekneva; T Quertermous; B W Christman; M L Lawrence; B Meyrick
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5.  Modulation of angiotensin II-induced vasoconstriction by endothelium-derived relaxing factor in the isolated microperfused rabbit afferent arteriole.

Authors:  S Ito; C S Johnson; O A Carretero
Journal:  J Clin Invest       Date:  1991-05       Impact factor: 14.808

6.  Inhibition of endothelial derived relaxing factor (EDRF) aggravates ischemic acute renal failure in anesthetized rats.

Authors:  M S Chintala; P J Chiu; S Vemulapalli; R W Watkins; E J Sybertz
Journal:  Naunyn Schmiedebergs Arch Pharmacol       Date:  1993-09       Impact factor: 3.000

Review 7.  The endothelial L-arginine/nitric oxide pathway and the renal circulation.

Authors:  T F Lüscher; H A Bock
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8.  Endothelium-derived relaxing factor inhibits transport and increases cGMP content in cultured mouse cortical collecting duct cells.

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  8 in total

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