This Article Full Text Full Text (PDF) All Versions of this Article: 52/1/137    most recent HYPERTENSIONAHA.108.111435v2 HYPERTENSIONAHA.108.111435v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Google Scholar Articles by Zhao, D. Articles by Navar, L. G. PubMed PubMed Citation Articles by Zhao, D. Articles by Navar, L. G. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Hazardous Substances DB SODIUM Related Collections Other hypertension

(Hypertension. 2008;52:137.)
© 2008 American Heart Association, Inc.

Original Articles

Acute Angiotensin II Infusions Elicit Pressure Natriuresis in Mice and Reduce Distal Fractional Sodium Reabsorption

From the Department of Physiology and Hypertension and Renal Center of Excellence, Tulane University School of Medicine, New Orleans, La.

Correspondence to L. Gabriel Navar, Department of Physiology SL-39, Tulane University Health Sciences Center, 1430 Tulane Ave, New Orleans, LA 70112. E-mail navar{at}tulane.edu

Acute angiotensin II (Ang II) infusions into mice increase arterial pressure (AP) and elicit pressure natriuresis. We used this model of pressure natriuresis to delineate the distal nephron responses to AP-mediated increases in distal sodium delivery. In the first group, we measured changes in urinary sodium excretion (U_NaV) in male C57/BL6 anesthetized mice (n=9) before and during acute Ang II infusions (5 ng/g of body weight per minute). Acute Ang II infusions increased AP (98±3 to 126±5 mm Hg; P<0.001), urine flow (2.7±0.5 to 6.0±0.8 µL/min; P<0.01), and U_NaV (0.6±0.2 to 1.3±0.2 µEq/min; P<0.05). There were significant relationships between U_NaV and urine flow (y=0.207x+0.030; P<0.0001) and between U_NaV and AP (y=0.027x–2.100). In a separate series, distal sodium delivery and fractional reabsorption of distal sodium delivery were determined in control (n=12) and Ang II–infused mice (n=8) by comparing U_NaV before and after blockade of the 2 major distal nephron sodium transporters with amiloride (5 mg/kg of body weight) plus bendroflumethiazide (12 mg/kg of body weight). A positive relationship was found between U_NaV (y=0.015x–1.100; P<0.0001) or distal sodium delivery (y=0.027x–0.900; P<0.0001) and AP. An inverse relationship was found between fractional reabsorption of distal sodium delivery and AP (y=–0.511x+128.300; P<0.01). These data indicate that Ang II–mediated pressure natriuresis involves an increase in distal sodium delivery combined with a reduced distal nephron fractional sodium reabsorption, suggesting that increased AP prevents the distal nephron transport mechanisms from accommodating the increased distal delivery.

Key Words: Ang II • arterial pressure • renal sodium reabsorption • distal nephron segments • amiloride • bendroflumethiazide • fractional distal sodium reabsorption