Intrarenal aminopeptidase N inhibition augments natriuretic responses to angiotensin III in angiotensin type 1 receptor-blocked rats.

Intrarenal aminopeptidase N inhibition augments natriuretic responses to angiotensin III in angiotensin type 1 receptor-blocked rats. Research Abstract Details 

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Intrarenal aminopeptidase N inhibition augments natriuretic responses to angiotensin III in angiotensin type 1 receptor-blocked rats. Abstract Text:

Shetal H Padia,Brandon A Kemp,Nancy L Howell,Helmy M Siragy,Marie-Claude Fournie-Zaluski,Bernard P Roques,Robert M Carey,

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 micromol/min in stepwise fashion to 0.11+/-0.01 micromol/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 mumol/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.

Intrarenal aminopeptidase N inhibition augments natriuretic responses to angiotensin III in angiotensin type 1 receptor-blocked rats. Publishing Authors By Initials

SH Padia,BA Kemp,NL Howell,HM Siragy,MC Fournie-Zaluski,BP Roques,RM Carey,

For similar heterocyclic compounds: heterocyclic compounds, 1-ring: azoles: tetrazoles research abstracts see: heterocyclic compounds: heterocyclic compounds, 1-ring: azoles: tetrazoles research

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Intrarenal aminopeptidase N inhibition augments natriuretic responses to angiotensin III in angiotensin type 1 receptor-blocked rats. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: Hypertension

VOLUME: 49

Page Numbers: 625-30

Journal Abbreviation: Hypertension

ISSN: 1524-4563

DAY: 26

MONTH: 12

YEAR: 2006

Intrarenal aminopeptidase N inhibition augments natriuretic responses to angiotensin III in angiotensin type 1 receptor-blocked rats. Information

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LANGUAGE: eng

NlmUniqueID: 7906255

Intrarenal aminopeptidase N inhibition augments natriuretic responses to angiotensin III in angiotensin type 1 receptor-blocked rats. Keywords Mesh Terms:

KEYWORDS: Tetrazoles

MESH TERMS: administration & dosage

Chemical & Substance for Abstract: Intrarenal aminopeptidase N inhibition augments natriuretic responses to angiotensin III in angiotensin type 1 receptor-blocked rats. Information

Substance Name: Antigens, CD13

Registry Number: EC 3.4.11.2

Grant and Affiliation Information for Intrarenal aminopeptidase N inhibition augments natriuretic responses to angiotensin III in angiotensin type 1 receptor-blocked rats.

AFFILIATION: Division of Endocrinology and Metabolism, University of Virginia Health System, Charlottesville, VA 22908-1414, USA.

Country: United States

AGENCY: United States NHLBI

GRANT: HL-65659

ACRONYM: HL

MEDLINETA: Hypertension

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