| Myocardial fibrosis, impaired coronary hemodynamics, and biventricular dysfunction in salt-loaded SHR. | |
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MedLine Citation:
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PMID: 16299266 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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Jasmina Varagic; Edward D Frohlich; Javier Díez; Dinko Susic; Jwari Ahn; Arantxa González; Begoña López |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2005-11-18 |
Journal Detail:
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Title: American journal of physiology. Heart and circulatory physiology Volume: 290 ISSN: 0363-6135 ISO Abbreviation: Am. J. Physiol. Heart Circ. Physiol. Publication Date: 2006 Apr |
Date Detail:
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Created Date: 2006-03-15 Completed Date: 2006-05-02 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 100901228 Medline TA: Am J Physiol Heart Circ Physiol Country: United States |
Other Details:
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Languages: eng Pagination: H1503-9 Citation Subset: IM |
Affiliation:
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Hypertension Research Laboratory, Ochsner Clinic Foundation, New Orleans, LA 70121, USA. jvaragic@ochsner.org |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Blood Pressure / drug effects Coronary Circulation / drug effects Coronary Disease / chemically induced, physiopathology* Endomyocardial Fibrosis / chemically induced, physiopathology* Hypertension / chemically induced*, physiopathology* Male Rats Rats, Inbred SHR Sodium Chloride, Dietary / adverse effects* Stroke Volume / drug effects Ventricular Dysfunction / chemically induced, physiopathology* |
| Chemical | |
Reg. No./Substance:
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0/Sodium Chloride, Dietary |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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