The second hypothetical mechanism of enhanced Ach-mediated vasodilatation could be the activation of profound smooth muscle -adrenergic receptor perivascular sympathetic nerves typical for hypertension, which in turns may further overstimulate endothelial KCa (KCa3.1) and increase Ca2+ concentrations transmitted from smooth muscle through myoendothelial gap junctions. This evidence concerns the gene KCNN4 and hypertensive disorder.