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: 290/4/H1503    most recent 00970.2005v1 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 Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (10) Citing Articles via Google Scholar Google Scholar Articles by Varagic, J. Articles by López, B. Search for Related Content PubMed PubMed Citation Articles by Varagic, J. Articles by López, B.

Myocardial fibrosis, impaired coronary hemodynamics, and biventricular dysfunction in salt-loaded SHR

¹Hypertension Research Laboratory, Ochsner Clinic Foundation, New Orleans, Louisiana; and ²Division of Cardiovascular Pathophysiology, Centre for Applied Medical Research, and ³Department of Cardiology and Cardiovascular Surgery, School of Medicine, University of Navarra, Pamplona, Spain

Submitted 12 September 2005 ; accepted in final form 14 November 2005

Arterial pressure in most experimental and clinical hypertensions is exacerbated by salt. The effects of salt excess on right and left ventricular (RV and LV, respectively) functions and their respective coronary vasodilatory responses have been less explored. We therefore examined the effects of 8 wk of NaCl excess (8% in food) on arterial pressure, RV and LV functions (maximal rate of increase and decrease of ventricular pressure; dP/dt_max and dP/dt_min), coronary hemodynamics (microspheres), and collagen content (hydroxyproline assay and collagen volume fraction) in young adult normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR), aged 16 wk by the end of the study. Prolonged salt excess in WKY and SHR elevated pressure only modestly, but it markedly increased LV mass, especially in SHR. Moreover, salt excess significantly impaired RV and LV diastolic function in SHR but only LV diastolic function in WKY rats. However, salt loading affected neither RV nor LV contractile function in both strains. Interstitial and perivascular collagen deposition was increased, whereas coronary vasodilatory responses to dipyridamole diminished in both ventricles in the salt-loaded SHR but not in WKY rats. Therefore, accumulation of ventricular collagen as well as altered myocardial perfusion importantly contributed to the development of salt-related RV and LV dysfunctions in this model of naturally occurring hypertension. The unique effects of salt loading on both ventricles in SHR, but not WKY rats, strongly suggest that nonhemodynamic mechanisms in hypertensive disease participate pathophysiologically with salt-loading hypertension. These findings point to the conclusion that the concept of "salt sensitivity" in hypertension is far more complex than simply its effects on arterial pressure or the LV.

sodium excess; left and right ventricular function; spontaneously hypertensive rats; Wistar-Kyoto rats

This article has been cited by other articles:

				H. Matsui, K. Ando, H. Kawarazaki, A. Nagae, M. Fujita, T. Shimosawa, M. Nagase, and T. Fujita Salt Excess Causes Left Ventricular Diastolic Dysfunction in Rats With Metabolic Disorder Hypertension, August 1, 2008; 52(2): 287 - 294. [Abstract] [Full Text] [PDF]

				J. Varagic, E. D. Frohlich, D. Susic, J. Ahn, L. Matavelli, B. Lopez, and J. Diez AT1 receptor antagonism attenuates target organ effects of salt excess in SHRs without affecting pressure Am J Physiol Heart Circ Physiol, February 1, 2008; 294(2): H853 - H858. [Abstract] [Full Text] [PDF]

				E. D. Frohlich The Salt Conundrum: A Hypothesis Hypertension, July 1, 2007; 50(1): 161 - 166. [Full Text] [PDF]