Key result
V2 vasopressin receptor gene transfer boosts local fractional shortening and global contractility in preclinical models.
Why the study?
Systemic AVP levels are increased in congestive heart failure causing reduced cardiac contractility via V1 receptors, and heterologous myocardial expression of V2 receptors could enhance contractility by activating adenylyl cyclase.
Does adenoviral gene transfer of the V2R into the myocardium increase cardiac contractility in vivo in rat or rabbit models?
Population
Rat or rabbit myocardium in vivo
Comparison
Gene transfer of human V2R adenovirus vs control virus-treated hearts
Design
Preclinical study with ultrasound-guided injection or transcoronary adenoviral delivery
Authors
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No immediate clinical implications in HF; leaves open therapeutic potential of V2R gene transfer in humans.
Does adenoviral gene transfer of the V2R into the myocardium increase cardiac contractility in vivo in rat or rabbit models?
Adenoviral gene transfer of the V2 vasopressin receptor into the myocardium increases cardiac contractility in vivo, suggesting a potential novel strategy for congestive heart failure therapy.
Weig et al. (2000) studied Congestive heart failure (animal model). Adenoviral gene transfer of the human V2 vasopressin receptor (Ad-V2R) vs. Control virus was evaluated on Cardiac contractility (contraction amplitude, local fractional shortening, and global contractility dP/dt(max)). Adenoviral gene transfer of the V2 vasopressin receptor into rat or rabbit myocardium significantly increased local fractional shortening and global contractility compared to control virus.
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