| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Departments of Cellular and Molecular Medicine and of Medicine, University of Ottawa Heart Institute, University of Ottawa, Ottawa, Ontario, Canada K1Y 4W7
To examine the role of the ventral anteroventral third ventricle (vAV3V) in the hypertension induced by chronic subcutaneous ouabain and intracerebroventricular hypertonic saline, neurons in this area were destroyed by microinjection of an excitotoxin, ibotenic acid. Sham-operated or lesioned Wistar rats were administered ouabain (50 µg/day) or placebo for 3 wk from subcutaneously implanted controlled release pellets or artificial cerebrospinal fluid (CSF) or CSF containing 0.8 mol/l NaCl (5 µl/h) infused intracerebroventricularly for 2 wk. At the end of the experiment, mean arterial pressure (MAP) and heart rate at rest and in response to ganglionic blockade by intravenous hexamethonium (30 mg/kg) were assessed. In rats infused with hypertonic saline, responses to air jet stress were also assessed. Baseline MAP in sham-operated rats receiving intracerebroventricular hypertonic saline or subcutaneous ouabain was significantly higher than in control rats (115 ± 1 vs. 97 ± 3 and 121 ± 3 vs. 103 ± 3 mmHg, respectively). vAV3V lesions abolished the increase in MAP elicited by chronic infusion of hypertonic saline or administration of ouabain. Sham-operated rats treated with hypertonic saline or ouabain exhibited significantly enhanced decreases in MAP to hexamethonium, but lesioned rats did not. Rats infused with hypertonic saline demonstrated enhanced responses to air jet stress that were similar in sham-operated and lesioned rats. These results demonstrate that neurons in the vAV3V are essential for the hypertension induced by intracerebroventricular hypertonic saline and subcutaneous ouabain, possibly by increasing sympathetic tone. Cardiovascular responses to air jet stress appear not to be mediated by the vAV3V.
hypertonic saline; excitotoxic lesion; air jet stress; ganglionic blockade
This article has been cited by other articles:
|
|
 |
|
  X. Hou, S. F. Theriault, I. Dostanic-Larson, A. E. Moseley, J. B Lingrel, H. Wu, S. Dean, and J. W. Van Huysse Enhanced pressor response to increased CSF sodium concentration and to central ANG I in heterozygous {alpha}2 Na+-K+-ATPase knockout mice Am J Physiol Regulatory Integrative Comp Physiol, May 1, 2009; 296(5): R1427 - R1438. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. N. Orlov and A. A. Mongin Salt-sensing mechanisms in blood pressure regulation and hypertension Am J Physiol Heart Circ Physiol, October 1, 2007; 293(4): H2039 - H2053. [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]
|
|
|
|
|
|
W. J. Cheung, M.-A. H. Kent, E. El-Shahat, H. Wang, J. Tan, R. White, and F. H. H. Leenen Central and peripheral renin-angiotensin systems in ouabain-induced hypertension Am J Physiol Heart Circ Physiol, August 1, 2006; 291(2): H624 - H630. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
I. Dostanic, R. J. Paul, J. N. Lorenz, S. Theriault, J. W. Van Huysse, and J. B. Lingrel The {alpha}2-isoform of Na-K-ATPase mediates ouabain-induced hypertension in mice and increased vascular contractility in vitro Am J Physiol Heart Circ Physiol, February 1, 2005; 288(2): H477 - H485. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Zhang and F. H. H. Leenen AT1 receptor blockers prevent sympathetic hyperactivity and hypertension by chronic ouabain and hypertonic saline Am J Physiol Heart Circ Physiol, March 1, 2001; 280(3): H1318 - H1323. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
