Sodium sensitivity of arterial blood pressure in L-NAME hypertensive but not eNOS knockout mice. Am J Hypertens 2006 Mar;19(3):327-9
Date
02/28/2006Pubmed ID
16500522DOI
10.1016/j.amjhyper.2005.09.012Scopus ID
2-s2.0-32944464810 (requires institutional sign-in at Scopus site) 17 CitationsAbstract
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.
Author List
Mattson DL, Meister CJMESH terms used to index this publication - Major topics in bold
AnimalsBlood Pressure
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
NG-Nitroarginine Methyl Ester
Nitric Oxide Synthase Type III
Sodium Chloride