Overexpression of endothelial β3 -adrenergic receptor induces diastolic dysfunction in rats.

ABSTRACT: Diastolic dysfunction is common in cardiovascular diseases, particularly in the case of heart failure with preserved ejection fraction. The challenge is to develop adequate animal models to envision human therapies in the future. It has been hypothesized that this diastolic dysfunction is linked to alterations in the nitric oxide (• NO) pathway. To investigate this issue further, we investigated the cardiac functions of a transgenic rat model (Tgβ3 ) that overexpresses the human β3 -adrenoceptor (hβ3 -AR) in the endothelium with the underlying rationale that the • NO pathway should be stimulated in the endothelium. Transgenic rats (Tgβ3 ) that express hβ3 -AR under the control of intercellular adhesion molecule 2 promoter were developed for a specific expression in endothelial cells. Trans

SUBMITTER: Dhot J 

PROVIDER: S-EPMC7754894 | biostudies-literature | 2020 Oct

REPOSITORIES: biostudies-literature