Renin-angiotensin system in the carotid body

Abstract

Research studies have been done on the influence of the renin-angiotensin system (RAS) on numerous tissues and organs. The local RAS, which is frequently of paracrine/autocrine origin, caters to specific organ and tissue needs through actions that add to, or differ from, the circulating RAS. Recent data have demonstrated a functional expression of RAS in the carotid body, wherein the carotid chemoreceptors play a major physiological role in the regulation of autonomic responses to changes in arterial chemical content. However, the angiotensin II and other vasoactive substances can directly modulate the excitability of the chemoreceptor. Long-term hypoxia modifies the level of gene expression in the carotid body by increasing the expression of AT(1) receptors along with sensitivity of the chemoreceptor to angiotensin II. Even though these findings support a physiological role of RAS in the carotid body, it has yet to be clearly defined. As a result this review will present current information about expression and localization of AT(1) receptors, and show that local RAS exists in the carotid body. The regulation of RAS by chronic hypoxia, the significance of its changes and clinical relevance in the carotid body, are also addressed.