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Articles in PresS, published online ahead of print August 29, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00475.2002
Submitted on June 6, 2002
Accepted on August 20, 2002
1 Internal Medicine, University of Arkansas for Medical Sciences, Little Rock, AR, USA; Pharmaceutical Sciences, University of Arkansas for Medical Sciences, Little Rock, AR, USA; Internal Medicine, Central Arkansas Veterans Healthcare System, Little Rock, AR, USA
2 Internal Medicine, Central Arkansas Veterans Healthcare System, Little Rock, AR, USA
3 Pathology, University of Arkansas for Medical Sciences, Little Rock, AR, USA
4 Surgery, University of Arkansas for Medical Sciences, Little Rock, AR, USA; Pathology, University of Arkansas for Medical Sciences, Little Rock, AR, USA
* To whom correspondence should be addressed. E-mail: josephjacob{at}uams.edu.
Hyperhomocysteinemia (Hhe), linked to cardiovascular disease by epidemiologic studies, may be an important factor in adverse cardiac remodeling in hypertension. Specifically, convergence of myocardial and vascular alterations promoted by Hhe and hypertension may exacerbate cardiac remodeling and myocardial dysfunction. We studied male spontaneously hypertensive rats fed one of three diets: control, intermediate Hhe-inducing, or severe Hhe-inducing. After 10 weeks of dietary intervention, cardiac function was assessed in vitro, and cardiac and coronary arteriolar remodeling were monitored by histomorphometric, immunohistochemical, and biochemical techniques. Results showed that Hhe induced a diastolic dysfunction, as characterized by the diastolic pressure-volume curve, without significant changes in baseline systolic function. Perivascular collagen levels were increased by Hhe, and there was an increase in left ventricular hydroxyproline levels. Myocyte size was not affected. Coronary arteriolar wall thickness increased with Hhe due to smooth muscle hyperplasia. Mast cells increased in parallel with Hhe and collagen accumulation. In summary, 10 weeks of Hhe caused coronary arteriolar remodeling, myocardial collagen deposition, and diastolic dysfunction in hypertensive rats.
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