Age-Related Changes in Blood Pressure in the Senescence-Accelerated Mouse (SAM): Aged SAMP1 Mice Manifest Hypertensive Vascular Disease
Abstract:Age-related changes in systolic blood pressure were assessed, using the senescence-accelerated mouse (SAM) model for aging research with strains SAMR1, SAMP1, and SAMP8. Each of the strains manifested a characteristic change in blood pressure with age. The SAMR1 strain, with normal aging, did not have chronologic changes from 2 to 27 months of age. The SAMP1 strain, with accelerated senescence, had a significant increase in blood pressure with age, and some (8 of 39) mice manifested hypertensive vascular disease characterized by high blood pressure, cardiac hypertrophy, and arteriolar fibrinoid necrosis at 11 to 14 months of age. The gradual increase in blood pressure after 8 to 10 months was considered to be preceded by progressive renal changes, from glomerulonephritis to contraction of the kidney, suggesting that the high blood pressure in the SAMP1 strain was of renal origin. Blood pressure in the SAMP8 strain, with age-related deficits in learning and memory, gradually decreased after 5 to 7 months of age, and was suggested to be due to the astrogliotic changes in response to spongiform degeneration in the medulla oblongata at 11 to 14 and 15 to 18 months of age.
Document Type: Research Article
Affiliations: 1: Department of Senescence Biology, Chest Disease Research Institute, Kyoto University, Kyoto 2: Department of Senescence Biology, Chest Disease Research Institute, Kyoto University, Sakyo-ku, Kyoto, 606 Japan 3: Department of Nutrition, Koshien University, Hyogo, Japan
Publication date: 1998-06-01
Comparative Medicine (CM), an international journal of comparative and experimental medicine, is the leading English-language publication in the field and is ranked by the Science Citation Index in the upper third of all scientific journals. The mission of CM is to disseminate high-quality, peer-reviewed information that expands biomedical knowledge and promotes human and animal health through the study of laboratory animal disease, animal models of disease, and basic biologic mechanisms related to disease in people and animals.
Attention Members: To access the full text of the articles, be sure you are logged in to the AALAS website.
Attention: please note, due to a temporary technical problem, reference linking within the content is not available at this time
- Editorial Board
- Information for Authors
- Submit a Paper
- Subscribe to this Title
- Membership Information
- Information for Advertisers
- For issues prior to 1998
- Institutional Subscription Activation
- Ingenta Connect is not responsible for the content or availability of external websites