Neural mechanisms of angiotensin II-salt hypertension: implications for therapies targeting neural control of the splanchnic circulation.

John W Osborn, Gregory D Fink, Marcos T Kuroki

Department of Integrative Biology and Physiology, University of Minnesota, 6-125 Jackson Hall, Minneapolis, MN 55455, USA. osbor003@umn.edu

Current hypertension reports 2011 Jun

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Chronically elevated plasma angiotensin II (AngII) causes a salt-sensitive form of hypertension that is associated with a differential pattern of peripheral sympathetic outflow. This "AngII-salt sympathetic signature" is characterized by a transient reduction in sympathetic nervous system activity (SNA) to the kidneys, no change in SNA to skeletal muscle, and a delayed activation of SNA to the splanchnic circulation. Studies suggest that the augmented sympathetic influence on the splanchnic vascular bed increases vascular resistance and decreases vascular capacitance, leading to hypertension via translocation of blood volume from the venous to the arterial circulation. This unique sympathetic signature is hypothesized to be generated by a balance of central excitatory inputs and differential baroreceptor inhibitory inputs to sympathetic premotor neurons in the rostral ventrolateral medulla. The relevance of these findings to human hypertension and the future development of targeted sympatholytic therapies are discussed.

Citation

John W Osborn, Gregory D Fink, Marcos T Kuroki. Neural mechanisms of angiotensin II-salt hypertension: implications for therapies targeting neural control of the splanchnic circulation. Current hypertension reports. 2011 Jun;13(3):221-8