Vascular Dysfunction in Rats with Diet-Induced Hyperhomocysteinemia: A Look at Hypertension

Student's Major

Chemistry and Geology

Student's College

Science, Engineering and Technology

Mentor's Name

Penny Knoblich

Mentor's Department

Biological Sciences

Mentor's College

Science, Engineering and Technology

Second Mentor's Name

James Rife

Second Mentor's Department

Biological Sciences

Second Mentor's College

Science, Engineering and Technology

Description

Elevation of plasma homocysteine levels is associated with stroke, peripheral vascular disease, myocardial infarction, and arteriosclerosis. The activation of DNA synthesis in vascular smooth muscle cells, combined with activation of coagulants and inactivatlon of anticoagulants and the ultimate production of free radicals in the blood, proposes several mechanisms for the atherosclerotic symptoms. Patients (n=357) with a C677->T mutation, resulting in a Val substitution for an Ala, in the methylenetetrahydrofolate enzyme involved in methionine metabolism show a decrease in hypertension when carrying the homozygous valine genotype. Ischemic stroke Patients (n=125) with and without hyperhomocysteinemia were tested for hypertension. Of the patients with hyperhomocysteinemia, 89% were reported to have hypertension. Based on previous studies we hypothesize that as homocysteine levels increase in rats, atherosclerotic-like conditions will follow, leading to increase plaque build-up and decreased elasticity, resulting in hypertension. Blood pressure will be measured by the tail-cuff method beginning at five weeks of age. Rats were mated randomly within their own breed, and will be placed on a homocysteine diet or a normal diet after weaning. Preliminary testing on the stability of homocysteine in water will be carried out prior to weaning.

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Vascular Dysfunction in Rats with Diet-Induced Hyperhomocysteinemia: A Look at Hypertension

Elevation of plasma homocysteine levels is associated with stroke, peripheral vascular disease, myocardial infarction, and arteriosclerosis. The activation of DNA synthesis in vascular smooth muscle cells, combined with activation of coagulants and inactivatlon of anticoagulants and the ultimate production of free radicals in the blood, proposes several mechanisms for the atherosclerotic symptoms. Patients (n=357) with a C677->T mutation, resulting in a Val substitution for an Ala, in the methylenetetrahydrofolate enzyme involved in methionine metabolism show a decrease in hypertension when carrying the homozygous valine genotype. Ischemic stroke Patients (n=125) with and without hyperhomocysteinemia were tested for hypertension. Of the patients with hyperhomocysteinemia, 89% were reported to have hypertension. Based on previous studies we hypothesize that as homocysteine levels increase in rats, atherosclerotic-like conditions will follow, leading to increase plaque build-up and decreased elasticity, resulting in hypertension. Blood pressure will be measured by the tail-cuff method beginning at five weeks of age. Rats were mated randomly within their own breed, and will be placed on a homocysteine diet or a normal diet after weaning. Preliminary testing on the stability of homocysteine in water will be carried out prior to weaning.