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1 Hypertension Research Group, Ochsner Clinic Foundation, New Orleans, LA, USA
2 Division of Cardiovascular Pathophysiology, Centre for Applied Medical Research, School of Medicine, University of Navarra, Pamplona, Spain; Department of Cardiology and Cardiovascular Surgery, School of Medicine, University of Navarra, Pamplona, Spain
3 Division of Cardiovascular Pathophysiology, Centre for Applied Medical Research, School of Medicine, University of Navarra, Pamplona, Spain
* To whom correspondence should be addressed. E-mail: jvaragic{at}ochsner.org.
Arterial pressure in most experimental and clinical hypertensions is exacerbated by salt. The effects of salt excess on right (RV) and left (LV) ventricular functions and their respective coronary vasodilatory responses have been less explored. We therefore examined the effects of 8 weeks NaCl excess (8% in food) on arterial pressure, RV and LV functions (maximal rate of increase and decrease of ventricular pressure; dP/dTmax and dP/dTmin), coronary hemodynamics (microspheres), and collagen content (hydroxyproline assay, collagen volume fraction) in young adult normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rats (aged 16 weeks at study end). 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 in the WKY. 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. Therefore, accumulation of ventricular collagen as well as altered myocardial perfusion importantly contributed to the development of salt-related RV as well as LV dysfunctions in this model of naturally-occurring hypertension. The unique effects of salt-loading on both ventricles in SHR, but not WKY, 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 then simply its effects on arterial pressure or the LV.
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