Mismatch between peripheral and central demands in salt-sensitive hypertensive Dahl rats

► Salt-sensitive hypertension is believed to have high sympathetic activity, but not really. ► Dahl model rats show up-regulated nNOS neuron activity which is one of central inhibitors. ► Central nNOS system is enhanced by not salt, not gene, but hypertension per se. ► Based on biological mission of arterial pressure, we provide an idea why hypertension occurs. Sympathetic nerve activity in essential hypertension, which accounts for 90% of all hypertension cases, is in general thought to be elevated regardless of whether there is salt sensitivity or insensitivity. The cause is thought to be an abnormality in the sympathetic center. On the other hand, neuronal nitric oxide synthase-expressing neurons that function to inhibit the sympathetic center are clearly activated in the salt-sensitive hypertensive Dahl rat model. How is this related to sympathetic hyperactivity and hypertension? Also, how is hypertension associated with peripheral vessel contractility and renal function? Human life is supported by the body's various essential functions. The circulatory system links all these functions into one system that cannot be separated. Blood pressure is the driving force of this circulatory system, and both the central and peripheral demands determine the output. We examined the ‘mismatch’ between these two sides and its association with hypertension.