Key result
Pregabalin normalized α2δ-1 and CaV1.2α1 surface expression, CaV1.2 current density, and vasoconstriction in myocytes and arteries of hypertensive rats to control levels.
Population
Spontaneously hypertensive rats (SHR) and Wistar-Kyoto controls (cerebral artery myocytes and arteries)
Comparison
Pregabalin (an α2δ-1 ligand) vs Wistar-Kyoto controls / untreated state
Design
Preclinical
Authors
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Hypothesis-generating for α2δ-1 targeting in hypertension; does not support clinical pregabalin use.
Targeting α2δ-1 with pregabalin reverses pathological CaV1.2 channel trafficking and induces cerebrovascular dilation in genetic hypertension.
Bannister et al. (2012) studied Genetic Hypertension. Pregabalin vs. Untreated hypertensive rats / Wistar-Kyoto controls was evaluated on CaV1.2 current density, surface expression, and vasoconstriction. Pregabalin normalized α2δ-1 and CaV1.2α1 surface expression, CaV1.2 current density, and vasoconstriction in myocytes and arteries of hypertensive rats to control levels.
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