Revised: November 14, 2013
Accepted: December 12, 2013
Published online: February 23, 2014
One likely mechanism of essential hypertension (EH) is increased sympathoexcitation due to abnormal functions in the cardiovascular center of the brain. Recent findings obtained using experimental animal models of EH have shown that abnormal inflammation in the cardiovascular center may contribute to the onset of hypertension. Inflammatory molecules such as cytokines and reactive oxygen species released from the inflamed vasculature and glial cells in the medulla oblongata and hypothalamus might directly or indirectly affect neuronal functions. This in turn could increase sympathetic nerve activity and consequently arterial pressure. Abnormal inflammatory responses in the brain could also be central mechanisms underlying angiotensin II-related EH. In this review, we present the current understanding of EH mechanisms with regard to inflammatory responses in the cardiovascular center.
Core tip: One likely mechanism of essential hypertension (EH) is increased sympathoexcitation due to abnormal functions in the cardiovascular center of the brain. Recent findings obtained using experimental animal models of EH have shown that abnormal inflammation in the cardiovascular center may contribute to the onset of hypertension. Angiotensin II-related EH is no exception to this idea. In this review, we present the current understanding of EH mechanisms with regard to inflammatory responses in the cardiovascular center.