In Vivo Analysis Of Angiotensin II-Induced Hypertension And Vascular Disease In Rats

Murine models of abdominal aortic aneurysms (AAA) are commonly used to study the pathogenesis of this disease. Rats are often used in laboratory studies because of their size and because they are more physiologically similar to humans than mice are. In this study, we subcutaneously implanted 9-week-old apolipoprotein E-deficient (apoE KO) rats with angiotensin II-filled pumps to study the effects of this vasoconstricting hormone on aneurysm development. Deletion of the apoE gene in mice causes excess lipid accumulation in the blood vessels, thereby increasing the likelihood of atherosclerotic lesions in the aorta. However, atherosclerotic plaque buildup was not evident when the rats consumed either normal chow or high fat diets, and no dissecting aneurysms were identified via ultrasound. We observed an average of 32.5 +/- 28.8 mmHg increase in systolic blood pressures as early as 4 days post-pump implantation and an increase of 54.2 +/- 25.9 mmHg from baseline 6 weeks after angiotensin II infusion began. This study shows that apoE KO rats can be valuable models for the physiological development of hypertension but not for dissecting suprarenal aneurysms. Future studies will focus on studying the effects of angiotensin II on the hearts of these genetically modified animals

Toward Automation of the Supine Pressor Test for Preeclampsia

Preeclampsia leads to increased risk of morbidity and mortality for both mother and fetus. Most previous studies have largely neglected mechanical compression of the left renal vein by the gravid uterus as a potential mechanism. In this study, we first used a murine model to investigate the pathophysiology of left renal vein constriction. The results indicate that prolonged renal vein stenosis after 14 days can cause renal necrosis and an increase in blood pressure (BP) of roughly 30 mmHg. The second part of this study aimed to automate a diagnostic tool, known as the supine pressor test (SPT), to enable pregnant women to assess their preeclampsia development risk. A positive SPT has been previously defined as an increase of at least 20 mmHg in diastolic BP when switching between left lateral recumbent and supine positions. The results from this study established a baseline BP increase between the two body positions in nonpregnant women and demonstrated the feasibility of an autonomous SPT in pregnant women. Our results demonstrate that there is a baseline increase in BP of roughly 10-14 mmHg and that pregnant women can autonomously perform the SPT. Overall, this work in both rodents and humans suggests that (1) stenosis of the left renal vein in mice leads to elevation in BP and acute renal failure, (2) nonpregnant women experience a baseline increase in BP when they shift from left lateral recumbent to supine position, and (3) the SPT can be automated and used autonomously

Automation of the Supine Pressor Test for Preeclampsia

Preeclampsia leads to increased risk of morbidity and mortality for both mother and fetus. Most previous studies have largely neglected mechanical compression of the left renal vein by the gravid uterus as a potential mechanism. In this study we first used a murine model to investigate the pathophysiology of left renal vein constriction. The results indicate that prolonged renal vein stenosis after 14 days can cause renal necrosis and an increase in blood pressure (BP) of roughly 30 mmHg. The second part of this study aimed to automate a diagnostic tool, known as the supine pressor test (SPT), to enable pregnant women to assess their preeclampsia development risk. A positive SPT has been previously defined as an increase of at least 20 mmHg in diastolic BP when switching between left lateral recumbent and supine positions. The results from this study established a baseline BP increase between the two body positions in non-pregnant female subjects and demonstrated the feasibility and utility of an automated SPT in pregnant women. Our results demonstrate that there is a baseline increase in BP of roughly 10-14 mmHg and that pregnant women can autonomously perform the SPT. Overall, this work in both rodents and humans suggests that 1) stenosis of the left renal vein in mice leads to elevation in BP and acute renal failure, 2) non-pregnant women experience a baseline increase in BP when they shift from left lateral recumbent to supine position, and 3) the SPT can be automated and used autonomously