The mechanisms underlying the increased contraction in Rgs1 deficient vessels and Ang II-mediated hypertension in Rgs1−/−ApoE−/− mice are likely to involve different signalling cascades involving both MAPK signalling and calcium influx, which are known to be activated downstream of the alpha-adrenergic receptor and AT1R. This evidence concerns the gene AGTR1 and hypertensive disorder.