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PLoS Curr. 2011 Nov 4;3:RRN1266. doi: 10.1371/currents.RRN1266.

Baroreceptor reflex dysfunction in the BACHD mouse model of Huntington's disease.

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  • 1Department of Psychiatry & Biobehavioral Sciences, Laboratory of Circadian and Sleep Medicine, University of California, Los Angeles, Los Angeles, CA, 90024 USA and Department of Physiology, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095-1751.

Abstract

Huntington's disease is a progressive, neurodegenerative disorder that presents with a triad of clinical symptoms, which include movement abnormalities, emotional disturbance and cognitive impairment. Recent studies reported dysfunction of the autonomic nervous system in Huntington's disease patients, which may contribute to the increased incidence of cardiovascular events in this patient population that often leads to death. We measured the baroreceptor reflex, a process dependent on proper autonomic function, in the BACHD mouse model of Huntington's disease. We found a blunted response of the baroreceptor reflex as well as significantly higher daytime blood pressure in BACHD mice compared to WT controls, which are both indications of autonomic dysfunction. BACHD mice had increased heart weight to tibia length ratios at 7 and 12 mo of age suggesting hypertrophic changes of the heart, which we speculate is a response to the increased blood pressure and aberrant baroreceptor reflex. Despite these structural changes, the hearts of BACHD mice continue to function normally as assessed by echocardiographic analysis. Studies of autonomic and cardiovascular function in BACHD mice may help elucidate the pathophysiology of Huntington's disease and aid in the development of clinical strategies to offset the incidence of fatal cardiovascular events in the Huntington's disease patient population.

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