dl-propargylglycine reduces blood pressure and renal injury but increases kidney weight in angiotensin-II infused rats

Hydrogen sulfide (H2S), carbon monoxide (CO) and nitric oxide (NO) share signaling and vasorelaxant properties and are involved in proliferation and apoptosis. Inhibiting NO production or availability induces hypertension and proteinuria, which is prevented by concomitant blockade of the H2S produci...

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Published in:Nitric oxide 2015-09, Vol.49, p.56-66
Main Authors: Oosterhuis, Nynke R., Frenay, Anne-Roos S., Wesseling, Sebastiaan, Snijder, Pauline M., Slaats, Gisela G., Yazdani, Saleh, Fernandez, Bernadette O., Feelisch, Martin, Giles, Rachel H., Verhaar, Marianne C., Joles, Jaap A., van Goor, Harry
Format: Article
Language:English
Subjects:
Acute Kidney Injury - chemically induced
Acute Kidney Injury - metabolism
Alkynes - administration & dosage
Alkynes - pharmacology
Angiotensin II - adverse effects
Angiotensin-II
Animals
Blood Pressure - drug effects
Cell Proliferation
DL-Propargylglycine
Glycine - administration & dosage
Glycine - analogs & derivatives
Glycine - pharmacology
Heme Oxygenase-1 - metabolism
Hydrogen sulfide
Hydrogen Sulfide - metabolism
Hypertension
Kidney - drug effects
Kidney - pathology
Kidney weight
Male
Nitric Oxide
Organ Size
Proteinuria
Rats
Rats, Sprague-Dawley
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container_title Nitric oxide
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creator Oosterhuis, Nynke R.
Frenay, Anne-Roos S.
Wesseling, Sebastiaan
Snijder, Pauline M.
Slaats, Gisela G.
Yazdani, Saleh
Fernandez, Bernadette O.
Feelisch, Martin
Giles, Rachel H.
Verhaar, Marianne C.
Joles, Jaap A.
van Goor, Harry
description Hydrogen sulfide (H2S), carbon monoxide (CO) and nitric oxide (NO) share signaling and vasorelaxant properties and are involved in proliferation and apoptosis. Inhibiting NO production or availability induces hypertension and proteinuria, which is prevented by concomitant blockade of the H2S producing enzyme cystathionine γ-lyase (CSE) by d,l-propargylglycine (PAG). We hypothesized that blocking H2S production ameliorates Angiotensin II (AngII)-induced hypertension and renal injury in a rodent model. Effects of concomitant administration of PAG or saline were therefore studied in healthy (CON) and AngII hypertensive rats. In CON rats, PAG did not affect systolic blood pressure (SBP), but slightly increased proteinuria. In AngII rats PAG reduced SBP, proteinuria and plasma creatinine (180 ± 12 vs. 211 ± 19 mmHg; 66 ± 35 vs. 346 ± 92 mg/24 h; 24 ± 6 vs. 47 ± 15 μmol/L, respectively; p 
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Inhibiting NO production or availability induces hypertension and proteinuria, which is prevented by concomitant blockade of the H2S producing enzyme cystathionine γ-lyase (CSE) by d,l-propargylglycine (PAG). We hypothesized that blocking H2S production ameliorates Angiotensin II (AngII)-induced hypertension and renal injury in a rodent model. Effects of concomitant administration of PAG or saline were therefore studied in healthy (CON) and AngII hypertensive rats. In CON rats, PAG did not affect systolic blood pressure (SBP), but slightly increased proteinuria. In AngII rats PAG reduced SBP, proteinuria and plasma creatinine (180 ± 12 vs. 211 ± 19 mmHg; 66 ± 35 vs. 346 ± 92 mg/24 h; 24 ± 6 vs. 47 ± 15 μmol/L, respectively; p &lt; 0.01). Unexpectedly, kidney to body weight ratio was increased in all groups by PAG (p &lt; 0.05). Renal injury induced by AngII was reduced by PAG (p &lt; 0.001). HO-1 gene expression was increased by PAG alone (p &lt; 0.05). PAG increased inner cortical tubular cell proliferation after 1 week and decreased outer cortical tubular nucleus number/field after 4 weeks. In vitro proximal tubular cell size increased after exposure to PAG. In summary, blocking H2S production with PAG reduced SBP and renal injury in AngII infused rats. Independent of the cardiovascular and renal effects, PAG increased HO-1 gene expression and kidney weight. PAG alone increased tubular cell size and proliferation in-vivo and in-vitro. Our results are indicative of a complex interplay of gasotransmitter signaling/action of mutually compensatory nature in the kidney. •dl-propargylglycine (PAG) abolished H2S production in the kidney.•PAG reduced systolic blood pressure and renal injury in angiotensin II-infused rats.•Independent of kidney function PAG increased kidney weight.•PAG increased tubular cell size and proliferation.</description><identifier>ISSN: 1089-8603</identifier><identifier>EISSN: 1089-8611</identifier><identifier>DOI: 10.1016/j.niox.2015.07.001</identifier><identifier>PMID: 26192363</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Acute Kidney Injury - chemically induced ; Acute Kidney Injury - metabolism ; Alkynes - administration &amp; dosage ; Alkynes - pharmacology ; Angiotensin II - adverse effects ; Angiotensin-II ; Animals ; Blood Pressure - drug effects ; Cell Proliferation ; DL-Propargylglycine ; Glycine - administration &amp; dosage ; Glycine - analogs &amp; derivatives ; Glycine - pharmacology ; Heme Oxygenase-1 - metabolism ; Hydrogen sulfide ; Hydrogen Sulfide - metabolism ; Hypertension ; Kidney - drug effects ; Kidney - pathology ; Kidney weight ; Male ; Nitric Oxide ; Organ Size ; Proteinuria ; Rats ; Rats, Sprague-Dawley</subject><ispartof>Nitric oxide, 2015-09, Vol.49, p.56-66</ispartof><rights>2015 Elsevier Inc.</rights><rights>Copyright © 2015 Elsevier Inc. 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Inhibiting NO production or availability induces hypertension and proteinuria, which is prevented by concomitant blockade of the H2S producing enzyme cystathionine γ-lyase (CSE) by d,l-propargylglycine (PAG). We hypothesized that blocking H2S production ameliorates Angiotensin II (AngII)-induced hypertension and renal injury in a rodent model. Effects of concomitant administration of PAG or saline were therefore studied in healthy (CON) and AngII hypertensive rats. In CON rats, PAG did not affect systolic blood pressure (SBP), but slightly increased proteinuria. In AngII rats PAG reduced SBP, proteinuria and plasma creatinine (180 ± 12 vs. 211 ± 19 mmHg; 66 ± 35 vs. 346 ± 92 mg/24 h; 24 ± 6 vs. 47 ± 15 μmol/L, respectively; p &lt; 0.01). Unexpectedly, kidney to body weight ratio was increased in all groups by PAG (p &lt; 0.05). Renal injury induced by AngII was reduced by PAG (p &lt; 0.001). HO-1 gene expression was increased by PAG alone (p &lt; 0.05). PAG increased inner cortical tubular cell proliferation after 1 week and decreased outer cortical tubular nucleus number/field after 4 weeks. In vitro proximal tubular cell size increased after exposure to PAG. In summary, blocking H2S production with PAG reduced SBP and renal injury in AngII infused rats. Independent of the cardiovascular and renal effects, PAG increased HO-1 gene expression and kidney weight. PAG alone increased tubular cell size and proliferation in-vivo and in-vitro. 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Inhibiting NO production or availability induces hypertension and proteinuria, which is prevented by concomitant blockade of the H2S producing enzyme cystathionine γ-lyase (CSE) by d,l-propargylglycine (PAG). We hypothesized that blocking H2S production ameliorates Angiotensin II (AngII)-induced hypertension and renal injury in a rodent model. Effects of concomitant administration of PAG or saline were therefore studied in healthy (CON) and AngII hypertensive rats. In CON rats, PAG did not affect systolic blood pressure (SBP), but slightly increased proteinuria. In AngII rats PAG reduced SBP, proteinuria and plasma creatinine (180 ± 12 vs. 211 ± 19 mmHg; 66 ± 35 vs. 346 ± 92 mg/24 h; 24 ± 6 vs. 47 ± 15 μmol/L, respectively; p &lt; 0.01). Unexpectedly, kidney to body weight ratio was increased in all groups by PAG (p &lt; 0.05). Renal injury induced by AngII was reduced by PAG (p &lt; 0.001). HO-1 gene expression was increased by PAG alone (p &lt; 0.05). PAG increased inner cortical tubular cell proliferation after 1 week and decreased outer cortical tubular nucleus number/field after 4 weeks. In vitro proximal tubular cell size increased after exposure to PAG. In summary, blocking H2S production with PAG reduced SBP and renal injury in AngII infused rats. Independent of the cardiovascular and renal effects, PAG increased HO-1 gene expression and kidney weight. PAG alone increased tubular cell size and proliferation in-vivo and in-vitro. Our results are indicative of a complex interplay of gasotransmitter signaling/action of mutually compensatory nature in the kidney. •dl-propargylglycine (PAG) abolished H2S production in the kidney.•PAG reduced systolic blood pressure and renal injury in angiotensin II-infused rats.•Independent of kidney function PAG increased kidney weight.•PAG increased tubular cell size and proliferation.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>26192363</pmid><doi>10.1016/j.niox.2015.07.001</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record>
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ispartof Nitric oxide, 2015-09, Vol.49, p.56-66
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source Elsevier
subjects Acute Kidney Injury - chemically induced
Acute Kidney Injury - metabolism
Alkynes - administration & dosage
Alkynes - pharmacology
Angiotensin II - adverse effects
Angiotensin-II
Animals
Blood Pressure - drug effects
Cell Proliferation
DL-Propargylglycine
Glycine - administration & dosage
Glycine - analogs & derivatives
Glycine - pharmacology
Heme Oxygenase-1 - metabolism
Hydrogen sulfide
Hydrogen Sulfide - metabolism
Hypertension
Kidney - drug effects
Kidney - pathology
Kidney weight
Male
Nitric Oxide
Organ Size
Proteinuria
Rats
Rats, Sprague-Dawley
title dl-propargylglycine reduces blood pressure and renal injury but increases kidney weight in angiotensin-II infused rats
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