This Article Full Text Full Text (PDF) All Versions of this Article: 48/4/658    most recent 01.HYP.0000238140.06251.7av1 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 O’Donaughy, T. L. Articles by Brooks, V. L. Search for Related Content PubMed PubMed Citation Articles by O’Donaughy, T. L. Articles by Brooks, V. L. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Medline Plus Health Information High Blood Pressure Hazardous Substances DB SODIUM CHLORIDE Related Collections Other hypertension

(Hypertension. 2006;48:658.)
© 2006 American Heart Association, Inc.

Original Articles

Central Action of Increased Osmolality to Support Blood Pressure in Deoxycorticosterone Acetate–Salt Rats

From the Department of Physiology and Pharmacology, Oregon Health & Science University, Portland.

Correspondence to Virginia L. Brooks, Department of Physiology and Pharmacology, L-334, Oregon Health & Science University, 3181 SW Sam Jackson Park Rd, Portland, OR 97239. E-mail brooksv{at}ohsu.edu

To test the hypothesis that increased osmolality contributes to hypertension in deoxycorticosterone acetate (DOCA)-salt–hypertensive rats by acting in the brain, DOCA-salt and Sham-salt rats were instrumented with bilateral, nonoccluding intracarotid and femoral catheters. Two weeks prior, rats were uninephrectomized and received subcutaneous implants with or without DOCA (65 mg) and began drinking salt water (1% NaCl and 0.2% KCl). DOCA-salt rats (n=28) exhibited elevated blood pressure (159±4 mm Hg; P<0.05) and heart rate (392±10 bpm; P<0.05) compared with Sham-salt animals (n=5; blood pressure: 107±5 mm Hg; heart rate: 355±10 bpm). Bilateral intracarotid infusion of hypotonic fluid (osmolality: 40 mOsm/L), which lowers osmolality of blood to the brain by 2%, rapidly decreased blood pressure in DOCA-salt rats (–22±4 mm Hg after 15 minutes; P<0.05; n=7) but not Sham-salt rats (2±2 mm Hg; n=5). Hypotonic fluid infused intravenously did not lower blood pressure (0±2 mm Hg) in DOCA-salt rats (n=7). In DOCA-salt rats pretreated with a V₁ vasopressin antagonist (Manning compound, 5 µg, IV), intracarotid hypotonic infusion still decreased blood pressure (–10±3 mm Hg; P<0.05; n=9), but the response was smaller (P<0.05). Finally, in DOCA-salt rats (n=4) pretreated with the V₁ antagonist and the ganglionic blocker hexamethonium, decreasing osmolality of blood to the brain did not reduce blood pressure. These data indicate that, in DOCA-salt rats, hypertonicity acts in the brain to support blood pressure, in part by stimulating vasopressin secretion and in part by stimulating another rapidly reversible mechanism, likely the sympathetic nervous system.

Key Words: hypertension, sodium-dependent • central nervous system • hypertension, mineralocorticoid • sodium • sympathetic nervous system • vasopressin

This article has been cited by other articles:

				Y. Wang, D. Babankova, J. Huang, G. M. Swain, and D. H. Wang Deletion of Transient Receptor Potential Vanilloid Type 1 Receptors Exaggerates Renal Damage in Deoxycorticosterone Acetate-Salt Hypertension Hypertension, August 1, 2008; 52(2): 264 - 270. [Abstract] [Full Text] [PDF]

				A. J. King, M. Novotny, G. M. Swain, and G. D. Fink Whole body norepinephrine kinetics in ANG II-salt hypertension in the rat Am J Physiol Regulatory Integrative Comp Physiol, April 1, 2008; 294(4): R1262 - R1267. [Abstract] [Full Text] [PDF]

				P. Shi, S. D. Stocker, and G. M. Toney Organum vasculosum laminae terminalis contributes to increased sympathetic nerve activity induced by central hyperosmolality Am J Physiol Regulatory Integrative Comp Physiol, December 1, 2007; 293(6): R2279 - R2289. [Abstract] [Full Text] [PDF]