LAUSR

Heart failure causes structural and functional impairment of cardiac tissue leading to cardiac dysfunction. Genetically hypertensive Schlager (BPH/2J) mice are a known model of high blood pressure with high sympathetic nerve activity. In this work we wanted to identify if Schlager mice can be a potential model to study hypertension induced heart failure development. Male and female adults (4-months; 4M) and middle aged (10 months; 10M) BPH/2J and their controls (BPN/3J) were used. Mean arterial pressure (MAP) was measured using the non-invasive blood pressure measurement system. Both male and female– 4M and 10M old– BPH/2J mice were found to have higher MAP compared to the control BPN/3J group. In male BPH/2J mice (4M and 10M of age), echocardiography revealed a reduction in ejection fraction and fractional shortening compared to the normotensive controls. In contrast, the female mice (both 4M and 10M of age) showed normal ejection fraction and fractional shortening. In this study, we found a significant reduction in the cardiac function and changes in cardiac structures hinting at hypertension induced structural changes in only the male Schlager mice. In future, we will study how high blood pressure, stress, and age impacts heart failure progression using the Schlager mice as a model. The study was supported by the Core Research Grant from the Anusandhan National Research Foundation, India. This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.