Journal
CURRENT HYPERTENSION REPORTS
Volume 13, Issue 3, Pages 221-228Publisher
SPRINGER
DOI: 10.1007/s11906-011-0188-9
Keywords
Neurogenic hypertension; Sympathetic nerve activity; Salt; Angiotensin II; Splanchnic nerve activity
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Funding
- NHLBI NIH HHS [R01 HL076312, R01 HL076312-05] Funding Source: Medline
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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.
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