Contribution of Central Nervous System to Hypertension: role of Angiotensin II and Nitric Oxide

The contribution of the central nervous system (CNS) to the development and maintenance of high blood pressure is well established. Increased activity of the sympathetic nervous system during hypertensive conditions has been demonstrated experimentally and clinically. Different types of dysregulation in CNS, as seen by alterations in neurotransmitter production and baroreceptor reflex function, have been detected in early stages of hypertension. It was demonstrated that centrally acting drugs such as a-methyldopa, clonidine or reserpine effectively lower blood pressure. Moreover, in animal experiments renal hypertension could be prevented by central chemical sympathectomy. And psychosocial stress-induced sustained hypertension is well-known present phenomenom. The biochemical mechanisms contributing to the blood pressure increase by means of CNS are however lesser-known. Since lowering of blood pressure by the inhibition of the renin-angiotensin-aldosterone system within peripheral but also central nervous system was documented by several studies, it seems that brain angiotensin II may play a key role in the contribution of CNS to hypertension. On the other hand, sufficient production of nitric oxide within the system may effectively prevent increase in blood pressure.