Nitric oxide formed by neuronal nitric oxide synthase (nNOS) in the brain, autonomic inhibitory (nitrergic) nerves, and heart plays important roles in the control of blood pressure. Activation of nitrergic nerves innervating the systemic vasculature elicits vasodilatation, decreases peripheral resistance, and lowers blood pressure. Impairment of nitrergic nerve function, as well as endothelial dysfunction, results in systemic and pulmonary hypertension and decreased regional blood flow. Blockade of nNOS activity in the brain, particularly the medulla and hypothalamus, causes systemic hypertension. Under hypertensive states, such as those in spontaneously hypertensive and Dahl salt-sensitive rats, the expression of the nNOS gene in the brain is increased; this appears to counteract the activated sympathetic function in the vasomotor center. The present article summarizes information concerning the modulation of systemic and pulmonary hypertension through nNOS-derived nitric oxide produced in the brain and periphery.