In support of our findings, it is well established that the contribution of nitric oxide to vasodilation decreases in resistance arteries and arterioles, and the contribution of nitric oxide–independent mechanisms to vasodilation increases, particularly potassium efflux (sometimes referred to as endothelium-derived hyperpolarizing factor [EDH]), in cardiovascular diseases such as hypertension (16). The gene discussed is GJB6; the disease is hypertensive disorder.