Abstract
Increased blood pressure is a consistent risk factor for the development of atherosclerotic diseases in humans, although the basis for this relationship is unknown. Genetically engineered mice are now commonly used to study mechanisms of atherosclerosis. More recently, blood pressure can be reliably measured in conscious mice using either tail cuff or telemetric techniques. Thus, mouse models permit the investigation of the complex interactions of blood pressure and atherogenesis. Most mouse models exhibiting hypertension have increased atherosclerotic lesion size, although there have been exceptions to these findings. Also, there are several reports that have used methods to decrease blood pressure and demonstrated reduced atherosclerosis. In contrast, there are many studies in which atherosclerosis has been altered without changes in blood pressure, and conversely, studies in which blood pressure changes did not alter atherosclerosis. Studies that have specifically defined the role of elevated systolic blood pressure on the development of atherosclerosis have uniformly demonstrated that pressure per se is not responsible for changes in lesion development. Thus, while increased systolic blood pressure is frequently associated with atherosclerosis, the stimulus for the hypertension appears to be the major determinant of atherogenesis rather than pressure per se. A consistent theme in the literature has been that perturbations of the renin angiotensin system display the strongest correlations between blood pressure and atherosclerosis.
Keywords: LDL receptor, Atherosclerotic Lesions, angiotensin, AT2 receptors, systolic blood pressure
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