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Am J Physiol Heart Circ Physiol 283: H2567-H2574, 2002. First published August 29, 2002; doi:10.1152/ajpheart.00475.2002
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Vol. 283, Issue 6, H2567-H2574, December 2002

Hyperhomocysteinemia leads to adverse cardiac remodeling in hypertensive rats

Jacob Joseph1,2, Abeer Washington2, Lija Joseph3, Laura Koehler2, Louis M. Fink3, Martin Hauer-Jensen3,4, and Richard H. Kennedy2

1 Departments of Internal Medicine, 2 Pharmaceutical Sciences, 3 Pathology and 4 Surgery, University of Arkansas for Medical Sciences and Central Arkansas Veterans Healthcare System, Little Rock, Arkansas 72205

Hyperhomocysteinemia (Hhe), linked to cardiovascular disease by epidemiological 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 wk 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 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 wk of Hhe caused coronary arteriolar remodeling, myocardial collagen deposition, and diastolic dysfunction in hypertensive rats.

homocysteine; diastolic dysfunction; collagen; interstitium; arteriole


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