Cardiovascular autonomic imbalance and baroreflex dysfunction in the apolipoprotein E-deficient mouse.

Genetically engineered mouse models and advances in molecular biotechnology have given extensive aid to experimental studies of cardiovascular mechanisms and dysfunction in pathological states such as atherosclerosis. Among the available animal models that have been developed to study atherosclerosis, the apolipoprotein E-deficient (apoE(-/-)) mouse is the most ideal genetically modified animal presently available. The apoE(-/-)mouse develops spontaneous severe hypercholesterolemia in a short-time and subsequently develops atherosclerotic lesions similar to those found in humans. Since its creation two decades ago, the apoE(-/-)mouse has greatly contributed to the understanding of atherosclerosis, but the consequences of hypercholesterolemia and atherosclerosis for the autonomic control of cardiovascular function in this mouse model have not been reviewed. In this article, we provide an overview of abnormalities of the parasympathetic and sympathetic nervous systems controlling heart rate and blood pressure and emphasize the dysfunction of the baroreflex control of cardiovascular function and how this dysfunction is influenced by nitric oxide, reactive oxygen species, aging and an atherogenic diet in the apoE(-/-)mouse.