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Impaired effect by NO synthase inhibition on tubuloglomerular feedback in rats after chronic renal denervation

Acute unilateral renal denervation (aDNX) is associated with reduced tubuloglomerular feedback (TGF) sensitivity. Six days after denervation (cDNX) TGF sensitivity is somewhat restored, but TGF reactivity increased. This study aimed to investigate if the increased TGF reactivity that was seen in cDN...

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Published in:Acta physiologica Scandinavica 2000, Vol.168 (1), p.89-93
Main Authors: THORUP, C, KURKUS, J, MORSING, P, OLLERSTAM, A, PERSSON, A. E. G
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PERSSON, A. E. G
description Acute unilateral renal denervation (aDNX) is associated with reduced tubuloglomerular feedback (TGF) sensitivity. Six days after denervation (cDNX) TGF sensitivity is somewhat restored, but TGF reactivity increased. This study aimed to investigate if the increased TGF reactivity that was seen in cDNX kidneys was owing to reduced production of nitric oxide (NO). TGF characteristics were determined with micropuncture experiments in anaesthetized rats, using the stop-flow pressure (PSF) technique. Maximal drop in PSF (DeltaPSF) was used as an index of TGF reactivity and the loop of Henle perfusion rate that elicited half-maximal DeltaPSF, the turning point (TP) was used as a measure of TGF sensitivity. In cDNX kidneys, TP was higher than in control rats (25.4 +/- 1.5 nL min-1 vs. 19.1 +/- 1.1 nL min-1), but clearly lower than in aDNX rats (37. 3 +/- 3.1 nL min-1). TGF was more reactive in cDNX rats (DeltaPSF=14. 7 +/- 1.1 mmHg) than in aDNX (7.9 +/- 1.1 mmHg) and control rats (9. 6 +/- 0.9 mmHg). Intratubular inhibition of NO synthase N omega-nitro-L-arginine (L-NA) in sham-DNX animals, decreased TP to 13.9 +/- 2.2 nL min-1 and DeltaPSF was increased with 92%. In cDNX kidneys TP was not significantly reduced by L-NA, and TGF reactivity was only moderately increased by 31%. Intratubular infusion of L-arginine (L-Arg) reduced DeltaPSF from 10.2 +/- 0.7 to 6.5 +/- 0.6 mmHg in sham-DNX kidneys, but TP was unaffected. In cDNX kidneys, there was no effect on either DeltaPSF or TP by the addition of L-Arg. However, when NO was delivered via sodium nitroprusside in the tubular perfusate, a clear reduction of DeltaPSF was seen in both sham-DNX and cDNX kidneys (from 9.9 +/- 0.5 to 4.4 +/- 1.0 and from14.9 +/- 1.3 to 8.1 +/- 1.5 mmHg, respectively). This indicates that cDNX is a state of low renal NO production and that this low level of NO resets TGF to a higher sensitivity and more pronounced reactivity.
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E. G</creatorcontrib><title>Impaired effect by NO synthase inhibition on tubuloglomerular feedback in rats after chronic renal denervation</title><title>Acta physiologica Scandinavica</title><addtitle>Acta Physiol Scand</addtitle><description>Acute unilateral renal denervation (aDNX) is associated with reduced tubuloglomerular feedback (TGF) sensitivity. Six days after denervation (cDNX) TGF sensitivity is somewhat restored, but TGF reactivity increased. This study aimed to investigate if the increased TGF reactivity that was seen in cDNX kidneys was owing to reduced production of nitric oxide (NO). TGF characteristics were determined with micropuncture experiments in anaesthetized rats, using the stop-flow pressure (PSF) technique. Maximal drop in PSF (DeltaPSF) was used as an index of TGF reactivity and the loop of Henle perfusion rate that elicited half-maximal DeltaPSF, the turning point (TP) was used as a measure of TGF sensitivity. 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Psychology</topic><topic>Kidney - innervation</topic><topic>Kidney Glomerulus - drug effects</topic><topic>Kidney Glomerulus - physiology</topic><topic>Kidney Tubules - drug effects</topic><topic>Kidney Tubules - physiology</topic><topic>Male</topic><topic>Nervous System Physiological Phenomena</topic><topic>Nitric Oxide Donors - pharmacology</topic><topic>Nitric Oxide Synthase - antagonists &amp; inhibitors</topic><topic>Nitric Oxide Synthase - physiology</topic><topic>Nitroarginine - pharmacology</topic><topic>Nitroprusside - pharmacology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Time Factors</topic><topic>Vertebrates: urinary system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>THORUP, C</creatorcontrib><creatorcontrib>KURKUS, J</creatorcontrib><creatorcontrib>MORSING, P</creatorcontrib><creatorcontrib>OLLERSTAM, A</creatorcontrib><creatorcontrib>PERSSON, A. E. 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G</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Impaired effect by NO synthase inhibition on tubuloglomerular feedback in rats after chronic renal denervation</atitle><jtitle>Acta physiologica Scandinavica</jtitle><addtitle>Acta Physiol Scand</addtitle><date>2000</date><risdate>2000</risdate><volume>168</volume><issue>1</issue><spage>89</spage><epage>93</epage><pages>89-93</pages><issn>0001-6772</issn><eissn>1365-201X</eissn><coden>APSCAX</coden><abstract>Acute unilateral renal denervation (aDNX) is associated with reduced tubuloglomerular feedback (TGF) sensitivity. Six days after denervation (cDNX) TGF sensitivity is somewhat restored, but TGF reactivity increased. This study aimed to investigate if the increased TGF reactivity that was seen in cDNX kidneys was owing to reduced production of nitric oxide (NO). TGF characteristics were determined with micropuncture experiments in anaesthetized rats, using the stop-flow pressure (PSF) technique. Maximal drop in PSF (DeltaPSF) was used as an index of TGF reactivity and the loop of Henle perfusion rate that elicited half-maximal DeltaPSF, the turning point (TP) was used as a measure of TGF sensitivity. In cDNX kidneys, TP was higher than in control rats (25.4 +/- 1.5 nL min-1 vs. 19.1 +/- 1.1 nL min-1), but clearly lower than in aDNX rats (37. 3 +/- 3.1 nL min-1). TGF was more reactive in cDNX rats (DeltaPSF=14. 7 +/- 1.1 mmHg) than in aDNX (7.9 +/- 1.1 mmHg) and control rats (9. 6 +/- 0.9 mmHg). Intratubular inhibition of NO synthase N omega-nitro-L-arginine (L-NA) in sham-DNX animals, decreased TP to 13.9 +/- 2.2 nL min-1 and DeltaPSF was increased with 92%. In cDNX kidneys TP was not significantly reduced by L-NA, and TGF reactivity was only moderately increased by 31%. Intratubular infusion of L-arginine (L-Arg) reduced DeltaPSF from 10.2 +/- 0.7 to 6.5 +/- 0.6 mmHg in sham-DNX kidneys, but TP was unaffected. In cDNX kidneys, there was no effect on either DeltaPSF or TP by the addition of L-Arg. However, when NO was delivered via sodium nitroprusside in the tubular perfusate, a clear reduction of DeltaPSF was seen in both sham-DNX and cDNX kidneys (from 9.9 +/- 0.5 to 4.4 +/- 1.0 and from14.9 +/- 1.3 to 8.1 +/- 1.5 mmHg, respectively). This indicates that cDNX is a state of low renal NO production and that this low level of NO resets TGF to a higher sensitivity and more pronounced reactivity.</abstract><cop>Oxford</cop><pub>Blackwell Science</pub><pmid>10691784</pmid><doi>10.1046/j.1365-201X.2000.00644.x</doi><tpages>5</tpages></addata></record>
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subjects Animals
Arginine - pharmacology
Biological and medical sciences
Denervation
Enzyme Inhibitors - pharmacology
Feedback - drug effects
Fundamental and applied biological sciences. Psychology
Kidney - innervation
Kidney Glomerulus - drug effects
Kidney Glomerulus - physiology
Kidney Tubules - drug effects
Kidney Tubules - physiology
Male
Nervous System Physiological Phenomena
Nitric Oxide Donors - pharmacology
Nitric Oxide Synthase - antagonists & inhibitors
Nitric Oxide Synthase - physiology
Nitroarginine - pharmacology
Nitroprusside - pharmacology
Rats
Rats, Sprague-Dawley
Time Factors
Vertebrates: urinary system
title Impaired effect by NO synthase inhibition on tubuloglomerular feedback in rats after chronic renal denervation
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