This review provides a critical evaluation of methodologies for assessing neurocardiovascular regulation in murine models, essential for understanding complex diseases like hypertension and heart failure.
May inform preclinical neurocardiovascular study design in mice; leaves open optimal translation to human hypertension and heart failure.
A growing body of evidence indicates that a number of common complex diseases, including hypertension, heart failure, and obesity, are characterized by alterations in central neurocardiovascular regulation. However, our understanding of how changes within the central nervous system contribute to the development and progression of these and other diseases remains unclear. As with many areas of cardiovascular research, the mouse has emerged as a key species for investigations of neuroregulatory processes because of its amenability to highly specific genetic manipulations. In parallel with the development of increasingly sophisticated murine models has come the miniaturization and advancement in methodologies for in vivo assessment of neurocardiovascular end points in the mouse. The following brief review will focus on a number of key direct and indirect experimental approaches currently in use, including measurement of arterial blood pressure, assessment of cardiovascular autonomic control, and evaluation of arterial baroreflex function. The advantages and limitations of each methodology are highlighted to allow for a critical evaluation by the reader when considering these approaches.
No takes yet. Share an insight, caveat, or question.
Young et al. (2011) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: