This Article Full Text Full Text (PDF) 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 Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Tan, D. Y. Articles by Manning, R. D. Search for Related Content PubMed PubMed Citation Articles by Tan, D. Y. Articles by Manning, R. D., Jr

(Hypertension. 1999;33:456-461.)
© 1999 American Heart Association, Inc.

Scientific Contribution

Role of Neuronal Nitric Oxide Synthase in Dahl Salt-Sensitive Hypertension

Dunyong Y. Tan; Shumei Meng; R. Davis Manning, Jr

From the Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Miss.

Correspondence to R. Davis Manning, Jr, Department of Physiology and Biophysics, 2500 North State St, Jackson, MS 39216. E-mail dmanning{at}physiology.umsmed.edu

Abstract—The goal of this study was to determine the role of neuronal nitric oxide synthase (nNOS) in the arterial pressure, renal hemodynamic, and renal excretory changes that occur in Dahl salt-resistant (DR) and salt-sensitive (DS) rats during changes in Na intake. Fifty-three DR and DS rats/Rapp strain of 7 to 8 weeks of age with indwelling arterial and venous catheters were subjected to low (0.87 mmol/d) or high (20.6 mmol/d) Na intake beginning 2 days before the start of the control period. Measurements were made during a 5-day control period followed by a 5-day period of nNOS inhibition with intravenous 7-nitroindazole (7NI, 1.67 mg · kg^-1 · h^-1) or vehicle infusion. After 5 days of 7NI, mean arterial pressure increased to 120±6% control in the DR-high Na, 7NI rats compared with 98±1% control (P<0.05) in the DR-high Na alone rats. After 5 days of 7NI, DS-high Na rats, which had a control arterial pressure 31 mm Hg higher than the comparable DR rats, increased their arterial pressure to 114±3% control, which was not significantly different from the DS-high Na alone pressure of 110±2% control. No significant changes occurred in glomerular filtration rate, effective renal plasma flow, urinary Na excretion, or urine volume because of 7NI. However, plasma renin activity decreased significantly in DR and DS rats on low Na intake with 7NI infusion. The data demonstrate that the highly salt-resistant DR rat became salt-sensitive during nNOS inhibition with 7NI. However, the arterial pressure of the DS rat was not affected by 7NI. This suggests that nitric oxide produced by nNOS in the DR rat normally helps to prevent salt-sensitive hypertension and that low functional levels of nNOS in the DS rat may contribute to its salt-sensitivity.

Key Words: arterial pressure • glomerular filtration rate • renal hemodynamics • sodium • renin • urine

This article has been cited by other articles:

				J. Li, J. White, L. Guo, X. Zhao, J. Wang, E. J. Smart, and X.-A. Li Salt Inactivates Endothelial Nitric Oxide Synthase in Endothelial Cells J. Nutr., March 1, 2009; 139(3): 447 - 451. [Abstract] [Full Text] [PDF]

				H. Castrop, F. Schweda, D. Mizel, Y. Huang, J. Briggs, A. Kurtz, and J. Schnermann Permissive role of nitric oxide in macula densa control of renin secretion Am J Physiol Renal Physiol, May 1, 2004; 286(5): F848 - F857. [Abstract] [Full Text] [PDF]

				S. Meng, G. W. Cason, A. W. Gannon, L. C. Racusen, and R. D. Manning Jr Oxidative Stress in Dahl Salt-Sensitive Hypertension Hypertension, June 1, 2003; 41(6): 1346 - 1352. [Abstract] [Full Text] [PDF]

				P. Ortiz, B. A. Stoos, N. J. Hong, D. M. Boesch, C. F. Plato, and J. L. Garvin High-Salt Diet Increases Sensitivity to NO and eNOS Expression But Not NO Production in THALs Hypertension, March 1, 2003; 41(3): 682 - 687. [Abstract] [Full Text] [PDF]

				N. Tian, A. W. Gannon, R. A. Khalil, and R. D. Manning Jr. Mechanisms of salt-sensitive hypertension: role of renal medullary inducible nitric oxide synthase Am J Physiol Regulatory Integrative Comp Physiol, February 1, 2003; 284(2): R372 - R379. [Abstract] [Full Text] [PDF]

				S. Meng, L. J. Roberts II, G. W. Cason, T. S. Curry, and R. D. Manning Jr. Superoxide dismutase and oxidative stress in Dahl salt-sensitive and -resistant rats Am J Physiol Regulatory Integrative Comp Physiol, September 1, 2002; 283(3): R732 - R738. [Abstract] [Full Text] [PDF]

				M. Szentivanyi Jr., A.-P. Zou, D. L. Mattson, P. Soares, C. Moreno, R. J. Roman, and A. W. Cowley Jr. Renal medullary nitric oxide deficit of Dahl S rats enhances hypertensive actions of angiotensin II Am J Physiol Regulatory Integrative Comp Physiol, July 1, 2002; 283(1): R266 - R272. [Abstract] [Full Text] [PDF]

				S. R. Abram, B. T. Alexander, W. A. Bennett, and J. P. Granger Role of neuronal nitric oxide synthase in mediating renal hemodynamic changes during pregnancy Am J Physiol Regulatory Integrative Comp Physiol, November 1, 2001; 281(5): R1390 - R1393. [Abstract] [Full Text] [PDF]

				L. Cervenka, H. J. Kramer, J. Maly, and J. Heller Role of nNOS in Regulation of Renal Function in Angiotensin II-Induced Hypertension Hypertension, August 1, 2001; 38(2): 280 - 285. [Abstract] [Full Text] [PDF]

				D. Y. Tan, S. Meng, G. W. Cason, and R. D. Manning Jr. Mechanisms of salt-sensitive hypertension: role of inducible nitric oxide synthase Am J Physiol Regulatory Integrative Comp Physiol, December 1, 2000; 279(6): R2297 - R2303. [Abstract] [Full Text] [PDF]