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Updated: Jul 16, 2026
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Published on: July 25, 2019
Hyperhomocysteinemia and myocardial expression of brain natriuretic peptide in rats
Markus Herrmann1, Omid Taban-Shoma, Ulrich Hübner
1Department of Clinical Chemistry, University Hospital of Saarland, Homburg/Saar, Germany.
Insights
Hyperhomocysteinemia (HHcy) in rats increased cardiac brain natriuretic peptide (BNP) expression. However, this HHcy did not lead to adverse cardiac remodeling in the heart.
Area of Science:
- Cardiology
- Biochemistry
- Toxicology
Background:
- Hyperhomocysteinemia (HHcy) is associated with impaired left ventricular function in chronic heart failure patients.
- HHcy may stimulate myocardial brain natriuretic peptide (BNP) expression and induce adverse cardiac remodeling.
Purpose of the Study:
- To investigate the effects of HHcy on cardiac BNP expression and left ventricular remodeling in a rat model.
- To determine if HHcy stimulates myocardial BNP expression and induces adverse left ventricular remodeling.
Main Methods:
- Fifty rats were randomized into five groups, with three groups receiving diets supplemented with methionine or homocystine to induce HHcy.
- After 12 weeks, plasma total homocysteine (tHcy) and BNP levels were measured, alongside histomorphometric analyses for cardiac remodeling.
- Control groups received a standard diet.
Main Results:
- Induced HHcy significantly increased plasma tHcy levels in the treatment groups compared to controls.
- Cardiac BNP expression was significantly elevated in rats with HHcy, particularly in the homocystine-supplemented groups.
- Histomorphometric analyses showed no significant differences in collagen deposition or mast cell infiltration, indicating no adverse cardiac remodeling.
Conclusions:
- Intermediate HHcy for three months stimulates increased cardiac BNP expression in rats.
- This increase in BNP expression was not accompanied by adverse cardiac remodeling.
Background:
Hyperhomocysteinemia (HHcy) has been linked to impaired left ventricular function and clinical class in patients with chronic heart failure. We hypothesized that HHcy stimulates myocardial brain natriuretic peptide (BNP) expression and induces adverse left ventricular remodeling.
Methods:
We randomized 50 rats into 5 groups. Groups Co1 and Co2 (controls) received a typical diet. Groups Meth, Hcy1, and Hcy2 were fed the same diet supplemented with 2.4% methionine, 1% homocystine, and 2% homocystine, respectively. After 12 weeks, we measured total plasma homocysteine (tHcy) and BNP in plasma and tissue, and we performed histomorphometric analyses.
Results:
All animals had comparable baseline body weight [mean (SD) 234 (26) g] and total circulating Hcy [4.7 (1.7) micromol/L]. After 12 weeks of treatment, total circulating Hcy increased in Meth, Hcy1, and Hcy2 [27.3 (8.8), 40.6 (7.0), and 54.0 (46.0) micromol/L, respectively] and remained unchanged in Co1 and Co2. Serum BNP significantly increased in 1 of 10 animals in Meth, 3 of 10 animals in Hcy1, and 3 of 10 animals in Hcy2. Median (25th-75th percentile) BNP tissue concentrations in Hcy1 and Hcy2 were 55% higher than in the corresponding controls [Co1 vs Hcy1, 225 (186-263) vs 338 (262-410) pg/mg protein, P = 0.05; Co2 vs Hcy2, 179 (107-261) vs 308 (192-429) pg/mg protein, P = 0.12]. In the Meth group, BNP expression was comparable to that of controls [200 (159-235) vs 225 (186-263) pg/mg protein, P = 0.32]. The percentage of perivascular and interstitial collagen and mast cell infiltration were comparable in all groups, indicating no adverse cardiac remodeling.
Conclusion:
Three months of intermediate HHcy stimulated increased cardiac BNP expression that was not accompanied by adverse cardiac remodeling.
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