Intrarenal Aminopeptidase N Inhibition Augments Natriuretic Responses to Angiotensin III in Angiotensin Type 1 Receptor–Blocked Rats
The renal angiotensin angiotensin type 2 receptor has been shown to mediate natriuresis, and angiotensin III, not angiotensin II, may be the preferential angiotensin type 2 receptor activator of this response. Angiotensin III is metabolized to angiotensin IV by aminopeptidase N. The present study hy...
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| Veröffentlicht in: | Hypertension (Dallas, Tex. 1979) Tex. 1979), 2007-03, Vol.49 (3, Part 2 Suppl), p.625-630 |
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| container_issue | 3, Part 2 Suppl |
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| container_title | Hypertension (Dallas, Tex. 1979) |
| container_volume | 49 |
| creator | Padia, Shetal H Kemp, Brandon A Howell, Nancy L Siragy, Helmy M Fournie-Zaluski, Marie-Claude Roques, Bernard P Carey, Robert M |
| description | The renal angiotensin angiotensin type 2 receptor has been shown to mediate natriuresis, and angiotensin III, not angiotensin II, may be the preferential angiotensin type 2 receptor activator of this response. Angiotensin III is metabolized to angiotensin IV by aminopeptidase N. The present study hypothesizes that inhibition of aminopeptidase N will augment natriuretic responses to intrarenal angiotensin III in angiotension type 1 receptor–blocked rats. Rats received systemic candesartan for 24 hours before the experiment. After a 1-hour control, cumulative renal interstitial infusion of angiotensin III at 3.5, 7, 14, and 28 nmol/kg per minute (each dose for 30 minutes) or angiotensin III combined with aminopeptidase N inhibitor PC-18 was administered into 1 kidney. The contralateral control kidney received renal interstitial infusion of vehicle. In kidneys infused with angiotensin III alone, renal sodium excretion rate increased from 0.05±0.01 μmol/min in stepwise fashion to 0.11±0.01 μmol/min at 28 nmol/kg per minute of angiotensin III (overall ANOVA F=3.68; P |
| doi_str_mv | 10.1161/01.HYP.0000254833.85106.4d |
| format | Article |
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Angiotensin III is metabolized to angiotensin IV by aminopeptidase N. The present study hypothesizes that inhibition of aminopeptidase N will augment natriuretic responses to intrarenal angiotensin III in angiotension type 1 receptor–blocked rats. Rats received systemic candesartan for 24 hours before the experiment. After a 1-hour control, cumulative renal interstitial infusion of angiotensin III at 3.5, 7, 14, and 28 nmol/kg per minute (each dose for 30 minutes) or angiotensin III combined with aminopeptidase N inhibitor PC-18 was administered into 1 kidney. The contralateral control kidney received renal interstitial infusion of vehicle. In kidneys infused with angiotensin III alone, renal sodium excretion rate increased from 0.05±0.01 μmol/min in stepwise fashion to 0.11±0.01 μmol/min at 28 nmol/kg per minute of angiotensin III (overall ANOVA F=3.68; P<0.01). In angiotensin III combined with PC-18, the renal sodium excretion rate increased from 0.05±0.01 to 0.32±0.08 μmol/min at 28 nmol/kg per minute of angiotensin III (overall ANOVA F=6.2; P<0.001). The addition of intrarenal PD-123319, an angiotensin type 2 receptor antagonist, to renal interstitial angiotensin III plus PC-18 inhibited the natriuretic response. Mean arterial blood pressure and renal sodium excretion rate from control kidneys were unchanged by angiotensin III ± PC-18 + PD-123319. Angiotensin III plus PC-18 induced a greater natriuretic response than Ang III alone (overall ANOVA F=16.9; P=0.0001). Aminopeptidase N inhibition augmented the natriuretic response to angiotensin III, suggesting that angiotensin III is a major agonist of angiotensin type 2 receptor–induced natriuresis.</description><identifier>ISSN: 0194-911X</identifier><identifier>EISSN: 1524-4563</identifier><identifier>DOI: 10.1161/01.HYP.0000254833.85106.4d</identifier><identifier>PMID: 17190872</identifier><identifier>CODEN: HPRTDN</identifier><language>eng</language><publisher>Philadelphia, PA: American Heart Association, Inc</publisher><subject>Angiotensin II Type 1 Receptor Blockers - administration & dosage ; Angiotensin III - pharmacology ; Animals ; Arterial hypertension. Arterial hypotension ; Benzimidazoles - administration & dosage ; Biological and medical sciences ; Blood and lymphatic vessels ; Cardiology. Vascular system ; CD13 Antigens - antagonists & inhibitors ; Clinical manifestations. Epidemiology. Investigative techniques. Etiology ; Enzyme Inhibitors - pharmacology ; Experimental diseases ; Medical sciences ; Methionine - analogs & derivatives ; Methionine - pharmacology ; Models, Animal ; Natriuresis - drug effects ; Natriuretic Agents - pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptors, Angiotensin - drug effects ; Sodium - urine ; Tetrazoles - administration & dosage</subject><ispartof>Hypertension (Dallas, Tex. 1979), 2007-03, Vol.49 (3, Part 2 Suppl), p.625-630</ispartof><rights>2007 American Heart Association, Inc.</rights><rights>2007 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5519-8748d398271252f641224b9f0a3522461ea29e5012c8e295272a6117ef9acb133</citedby><cites>FETCH-LOGICAL-c5519-8748d398271252f641224b9f0a3522461ea29e5012c8e295272a6117ef9acb133</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>309,310,314,777,781,786,787,3674,23911,23912,25121,27905,27906</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18625639$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17190872$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Padia, Shetal H</creatorcontrib><creatorcontrib>Kemp, Brandon A</creatorcontrib><creatorcontrib>Howell, Nancy L</creatorcontrib><creatorcontrib>Siragy, Helmy M</creatorcontrib><creatorcontrib>Fournie-Zaluski, Marie-Claude</creatorcontrib><creatorcontrib>Roques, Bernard P</creatorcontrib><creatorcontrib>Carey, Robert M</creatorcontrib><title>Intrarenal Aminopeptidase N Inhibition Augments Natriuretic Responses to Angiotensin III in Angiotensin Type 1 Receptor–Blocked Rats</title><title>Hypertension (Dallas, Tex. 1979)</title><addtitle>Hypertension</addtitle><description>The renal angiotensin angiotensin type 2 receptor has been shown to mediate natriuresis, and angiotensin III, not angiotensin II, may be the preferential angiotensin type 2 receptor activator of this response. Angiotensin III is metabolized to angiotensin IV by aminopeptidase N. The present study hypothesizes that inhibition of aminopeptidase N will augment natriuretic responses to intrarenal angiotensin III in angiotension type 1 receptor–blocked rats. Rats received systemic candesartan for 24 hours before the experiment. After a 1-hour control, cumulative renal interstitial infusion of angiotensin III at 3.5, 7, 14, and 28 nmol/kg per minute (each dose for 30 minutes) or angiotensin III combined with aminopeptidase N inhibitor PC-18 was administered into 1 kidney. The contralateral control kidney received renal interstitial infusion of vehicle. In kidneys infused with angiotensin III alone, renal sodium excretion rate increased from 0.05±0.01 μmol/min in stepwise fashion to 0.11±0.01 μmol/min at 28 nmol/kg per minute of angiotensin III (overall ANOVA F=3.68; P<0.01). In angiotensin III combined with PC-18, the renal sodium excretion rate increased from 0.05±0.01 to 0.32±0.08 μmol/min at 28 nmol/kg per minute of angiotensin III (overall ANOVA F=6.2; P<0.001). The addition of intrarenal PD-123319, an angiotensin type 2 receptor antagonist, to renal interstitial angiotensin III plus PC-18 inhibited the natriuretic response. Mean arterial blood pressure and renal sodium excretion rate from control kidneys were unchanged by angiotensin III ± PC-18 + PD-123319. Angiotensin III plus PC-18 induced a greater natriuretic response than Ang III alone (overall ANOVA F=16.9; P=0.0001). Aminopeptidase N inhibition augmented the natriuretic response to angiotensin III, suggesting that angiotensin III is a major agonist of angiotensin type 2 receptor–induced natriuresis.</description><subject>Angiotensin II Type 1 Receptor Blockers - administration & dosage</subject><subject>Angiotensin III - pharmacology</subject><subject>Animals</subject><subject>Arterial hypertension. Arterial hypotension</subject><subject>Benzimidazoles - administration & dosage</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Cardiology. Vascular system</subject><subject>CD13 Antigens - antagonists & inhibitors</subject><subject>Clinical manifestations. Epidemiology. Investigative techniques. Etiology</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Experimental diseases</subject><subject>Medical sciences</subject><subject>Methionine - analogs & derivatives</subject><subject>Methionine - pharmacology</subject><subject>Models, Animal</subject><subject>Natriuresis - drug effects</subject><subject>Natriuretic Agents - pharmacology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptors, Angiotensin - drug effects</subject><subject>Sodium - urine</subject><subject>Tetrazoles - administration & dosage</subject><issn>0194-911X</issn><issn>1524-4563</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpNkc9u1DAQhy0EosvCKyALCW4JHsf5Y25LBTRSVVBVJDhZ3mTSNU3sYDuqeuPEC_CGPAlud6XFPow1-mZ-kj9CXgHLASp4yyA_-_4lZ-nwUjRFkTclsCoX_SOygpKLTJRV8ZisGEiRSYBvJ-RZCD8YAyFE_ZScQA2SNTVfkd-tjV57tHqkm8lYN-McTa8D0gva2p3ZmmicpZvlekIbA73Q0ZvFYzQdvcQwOxsw0Ojoxl4bF9EGY2nbtjSV_1tXdzNSSCNdCnD-768_70fX3WBPL3UMz8mTQY8BXxzqmnz9-OHq9Cw7__ypPd2cZ11ZgsyaWjR9IRteAy_5UAngXGzlwHRRplcFqLnEkgHvGuSy5DXXFUCNg9TdFopiTd7s987e_VwwRDWZ0OE4aotuCaqSDIoq3TV5twc770LwOKjZm0n7OwVM3VtQDFSyoI4W1IMFJfo0_PKQsmwn7I-jh29PwOsDoEOnx8Fr25lw5JqKJ4MycWLP3boxog8343KLXu1Qj3H3EC141WScsZoVSW9235LFP8sVoX0</recordid><startdate>200703</startdate><enddate>200703</enddate><creator>Padia, Shetal H</creator><creator>Kemp, Brandon A</creator><creator>Howell, Nancy L</creator><creator>Siragy, Helmy M</creator><creator>Fournie-Zaluski, Marie-Claude</creator><creator>Roques, Bernard P</creator><creator>Carey, Robert M</creator><general>American Heart Association, Inc</general><general>Lippincott</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>200703</creationdate><title>Intrarenal Aminopeptidase N Inhibition Augments Natriuretic Responses to Angiotensin III in Angiotensin Type 1 Receptor–Blocked Rats</title><author>Padia, Shetal H ; Kemp, Brandon A ; Howell, Nancy L ; Siragy, Helmy M ; Fournie-Zaluski, Marie-Claude ; Roques, Bernard P ; Carey, Robert M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5519-8748d398271252f641224b9f0a3522461ea29e5012c8e295272a6117ef9acb133</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Angiotensin II Type 1 Receptor Blockers - administration & dosage</topic><topic>Angiotensin III - pharmacology</topic><topic>Animals</topic><topic>Arterial hypertension. Arterial hypotension</topic><topic>Benzimidazoles - administration & dosage</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Cardiology. Vascular system</topic><topic>CD13 Antigens - antagonists & inhibitors</topic><topic>Clinical manifestations. Epidemiology. Investigative techniques. 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Angiotensin III is metabolized to angiotensin IV by aminopeptidase N. The present study hypothesizes that inhibition of aminopeptidase N will augment natriuretic responses to intrarenal angiotensin III in angiotension type 1 receptor–blocked rats. Rats received systemic candesartan for 24 hours before the experiment. After a 1-hour control, cumulative renal interstitial infusion of angiotensin III at 3.5, 7, 14, and 28 nmol/kg per minute (each dose for 30 minutes) or angiotensin III combined with aminopeptidase N inhibitor PC-18 was administered into 1 kidney. The contralateral control kidney received renal interstitial infusion of vehicle. In kidneys infused with angiotensin III alone, renal sodium excretion rate increased from 0.05±0.01 μmol/min in stepwise fashion to 0.11±0.01 μmol/min at 28 nmol/kg per minute of angiotensin III (overall ANOVA F=3.68; P<0.01). In angiotensin III combined with PC-18, the renal sodium excretion rate increased from 0.05±0.01 to 0.32±0.08 μmol/min at 28 nmol/kg per minute of angiotensin III (overall ANOVA F=6.2; P<0.001). The addition of intrarenal PD-123319, an angiotensin type 2 receptor antagonist, to renal interstitial angiotensin III plus PC-18 inhibited the natriuretic response. Mean arterial blood pressure and renal sodium excretion rate from control kidneys were unchanged by angiotensin III ± PC-18 + PD-123319. Angiotensin III plus PC-18 induced a greater natriuretic response than Ang III alone (overall ANOVA F=16.9; P=0.0001). Aminopeptidase N inhibition augmented the natriuretic response to angiotensin III, suggesting that angiotensin III is a major agonist of angiotensin type 2 receptor–induced natriuresis.</abstract><cop>Philadelphia, PA</cop><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>17190872</pmid><doi>10.1161/01.HYP.0000254833.85106.4d</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Angiotensin II Type 1 Receptor Blockers - administration & dosage Angiotensin III - pharmacology Animals Arterial hypertension. Arterial hypotension Benzimidazoles - administration & dosage Biological and medical sciences Blood and lymphatic vessels Cardiology. Vascular system CD13 Antigens - antagonists & inhibitors Clinical manifestations. Epidemiology. Investigative techniques. Etiology Enzyme Inhibitors - pharmacology Experimental diseases Medical sciences Methionine - analogs & derivatives Methionine - pharmacology Models, Animal Natriuresis - drug effects Natriuretic Agents - pharmacology Rats Rats, Sprague-Dawley Receptors, Angiotensin - drug effects Sodium - urine Tetrazoles - administration & dosage |
| title | Intrarenal Aminopeptidase N Inhibition Augments Natriuretic Responses to Angiotensin III in Angiotensin Type 1 Receptor–Blocked Rats |
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