Medical Journals

Sodium Sensitivity of Arterial Blood Pressure in L-name Hypertensive but Not Enos Knockout Mice.

Authors:
  • Mattson David L
  • Meister Carla J

From: Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA. dmattson@mcw.edu

American journal of hypertension : journal of the American Society of Hypertension

  • Publish Date: Mar 2006
  • ISSN: 0895-7061
  • Volume: 19
  • Issue: 3
  • Pages: 327-9
  • Medium: Print
  • Language: English
  • Citation (JAMA): Mattson David L, Meister Carla J, et al. Sodium Sensitivity of Arterial Blood Pressure in L-name Hypertensive but Not Enos Knockout Mice.. Am. J. Hypertens. Mar 2006;19:327-9

Abstract

The present studies determined the sensitivity of mean arterial pressure (MAP) to sodium intake in endothelial nitric oxide synthase (eNOS) knockout mice, wild-type mice (C56BL/6J), and wild-type mice intravenously administered the nonspecific NOS inhibitor N(G)-nitro-l-arginine methyl ester (L-NAME, 8.6 mg/kg/d). Arterial blood pressure was measured from chronically implanted femoral arterial catheters in conscious, freely moving mice. The MAP was unaltered from the low sodium ( approximately 200 microEq/d) intake level of 106 +/- 3 mm Hg in wild-type mice when sodium intake was increased to approximately 1000 microEq/d (n = 12). Chronic administration of L-NAME to wild-type mice led to a sodium-dependent increase in MAP from 111 +/- 7 mm Hg to 124 +/- 5 mm Hg when the mice were placed on an elevated sodium intake (n = 7). In contrast to the L-NAME-treated mice, MAP was unaltered in eNOS knockout mice (n = 8) when sodium intake was increased (128 +/- 3 mm Hg v 129 +/- 5 mm Hg). These experiments demonstrate that eNOS knockout and L-NAME-treated wild-type mice are hypertensive relative to wild-type controls when sodium intake is elevated, but only L-NAME-treated mice exhibited a sodium-sensitive increase in MAP. Therefore, nitric oxide produced by eNOS does not appear to be important in the physiologic adaptation to elevated sodium chloride intake.

Mesh Headings (Keywords): Animals, Blood Pressure, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, NG-Nitroarginine Methyl Ester, Nitric Oxide Synthase Type III, Sodium Chloride


Check for Full Text / PubMed Unique Identifier (PMID): 16500522


This abstract is part of PubMed, a service of the U.S. National Library of Medicine. PubMed includes more than 17 million citations from MEDLINE and other life science journals for biomedical articles. See Copyright and Disclaimers.

Linked medical terms appearing on this page are added by Healia to help readers find more information and are not part of the original PubMed document.

The data herein was last updated on July 8th, 2008 and may not reflect the most current and accurate data available from NLM.


Advertisements

About | Privacy Policy | Business Solutions | Advertise | Contact | Add Healia to your site

©2012. Healia / Meredith Corporation  

Use of this site constitutes acceptance of our Terms of Service and Privacy Policy. All content on this Web site, including medical opinion and any other health-related information, is for informational purposes only and should not be used for a specific diagnosis or individual treatment plan for any situation. Use of this site and the information contained herein does not create a doctor-patient relationship. Always seek the direct advice of your doctor in connection with any questions or issues you may have regarding your own health or the health of others.