HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 288/2/H517    most recent 00651.2004v1 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 ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (10) Citing Articles via Google Scholar Google Scholar Articles by Huang, B. S. Articles by Leenen, F. H. H. Search for Related Content PubMed PubMed Citation Articles by Huang, B. S. Articles by Leenen, F. H. H.

Chronic central infusion of aldosterone leads to sympathetic hyperreactivity and hypertension in Dahl S but not Dahl R rats

Hypertension Unit, University of Ottawa Heart Institute, Ottawa, Ontario, Canada

Submitted 30 June 2004 ; accepted in final form 27 September 2004

Six-week-old Dahl salt-sensitive (S) and -resistant (R) rats received for 2 wk an intracerebroventricular infusion of aldosterone (Aldo) (22.5 ng/h) or vehicle containing artificial cerebrospinal fluid (aCSF) with 0.15 M Na⁺. At 8 wk, mean arterial pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA) were recorded in conscious rats at rest, in response to air stress, and to an intracerebroventricular injection of the ₂-adrenoceptor agonists guanabenz or ouabain. Baroreflex control of RSNA and HR was estimated by using intravenous phenylephrine and nitroprusside. In Dahl S but not Dahl R rats, Aldo raised resting MAP by 20–25 mmHg, doubled sympathoexcitatory and pressor responses to air stress and sympathoinhibitory and depressor responses to guanabenz, and impaired baroreflex function. In Dahl S but not Dahl R rats, Aldo significantly increased content of ouabain-like compounds (OLC) in the hypothalamus and attenuated excitatory responses to ouabain. Aldo did not affect water intake, plasma electrolytes, or OLC in plasma and adrenal glands. In another set of three groups of Dahl S rats, Aldo dissolved in aCSF containing 0.16, 0.15, or 0.14 M Na⁺ was infused intracerebroventricularly for 2 wk. CSF Na⁺ concentration ([Na⁺]) showed only a nonsignificant increase, but resting MAP increased from 111 ± 3 mmHg in rats with Aldo in 0.14 M Na⁺ to 131 ± 3 and 147 ± 3 mmHg with Aldo in 0.15 and 0.16 M Na⁺, respectively (P < 0.05 for both). These findings indicate that in Dahl S rats, intracerebroventricular infusion of Aldo causes similar central responses as high salt intake, i.e., increases in brain OLC content, sympathetic hyperreactivity, and hypertension. The extent of the increase in blood pressure (BP) by intracerebroventricular Aldo depends on the [Na⁺] in the vehicle. In Dahl R rats, intracerebroventricular Aldo did not increase brain OLC, sympathetic reactivity, and BP, suggesting that in this rat strain, a decrease in central responsiveness to mineralocorticoids may contribute to its salt-resistant nature.

ouabain-like compounds; cerebrospinal fluid Na⁺ concentration

This article has been cited by other articles:

				B. S. Huang, R. A. White, M. Ahmad, A. Y. Jeng, and F. H. H. Leenen Central infusion of aldosterone synthase inhibitor prevents sympathetic hyperactivity and hypertension by central Na+ in Wistar rats Am J Physiol Regulatory Integrative Comp Physiol, July 1, 2008; 295(1): R166 - R172. [Abstract] [Full Text] [PDF]

				F. Yao, C. Sumners, S. T. O'Rourke, and C. Sun Angiotensin II increases GABAB receptor expression in nucleus tractus solitarii of rats Am J Physiol Heart Circ Physiol, June 1, 2008; 294(6): H2712 - H2720. [Abstract] [Full Text] [PDF]

				Z.-H. Zhang, Y. Yu, Y.-M. Kang, S.-G. Wei, and R. B. Felder Aldosterone acts centrally to increase brain renin-angiotensin system activity and oxidative stress in normal rats Am J Physiol Heart Circ Physiol, February 1, 2008; 294(2): H1067 - H1074. [Abstract] [Full Text] [PDF]

				W. Schoner and G. Scheiner-Bobis Endogenous and exogenous cardiac glycosides: their roles in hypertension, salt metabolism, and cell growth Am J Physiol Cell Physiol, August 1, 2007; 293(2): C509 - C536. [Abstract] [Full Text] [PDF]

				C. B. Eap, M. Bochud, R. C. Elston, P. Bovet, M. P. Maillard, J. Nussberger, L. Schild, C. Shamlaye, and M. Burnier CYP3A5 and ABCB1 Genes Influence Blood Pressure and Response to Treatment, and Their Effect Is Modified by Salt Hypertension, May 1, 2007; 49(5): 1007 - 1014. [Abstract] [Full Text] [PDF]

				D. A. Scheuer, A. G. Bechtold, and K. A. Vernon Chronic Activation of Dorsal Hindbrain Corticosteroid Receptors Augments the Arterial Pressure Response to Acute Stress Hypertension, January 1, 2007; 49(1): 127 - 133. [Abstract] [Full Text] [PDF]

				V. L. Brooks, K. L. Freeman, and Y. Qi Time course of synergistic interaction between DOCA and salt on blood pressure: roles of vasopressin and hepatic osmoreceptors Am J Physiol Regulatory Integrative Comp Physiol, December 1, 2006; 291(6): R1825 - R1834. [Abstract] [Full Text] [PDF]

				B. S. Huang, W. J. Cheung, H. Wang, J. Tan, R. A. White, and F. H. H. Leenen Activation of brain renin-angiotensin-aldosterone system by central sodium in Wistar rats Am J Physiol Heart Circ Physiol, September 1, 2006; 291(3): H1109 - H1117. [Abstract] [Full Text] [PDF]

				A. G. Bechtold and D. A. Scheuer Glucocorticoids act in the dorsal hindbrain to modulate baroreflex control of heart rate Am J Physiol Regulatory Integrative Comp Physiol, April 1, 2006; 290(4): R1003 - R1011. [Abstract] [Full Text] [PDF]

				M. P. Blaustein, J. Zhang, L. Chen, and B. P. Hamilton How does salt retention raise blood pressure? Am J Physiol Regulatory Integrative Comp Physiol, March 1, 2006; 290(3): R514 - R523. [Abstract] [Full Text] [PDF]