We recently showed that K+-dependent electrical mechanism responsible for linking neuronal activity with upstream vasodilation is impaired at both capillary and arteriolar levels in a mouse model of hypertension (13) and at the capillary level in the 5xFAD mouse model of AD (14) as a result of compromised Kir2.1 function. The gene discussed is KCNJ2; the disease is hypertensive disorder.