Abstract
Activation of the sympathetic nervous system (SNS) stimulates renin release from the juxtraglomerular cells of the kidneys that leads to the generation of angiotensin I, which is then converted to angiotensin II (Ang II), the major effector peptide of the renin-angiotensin system (RAS). The formed Ang II can facilitate noradrenaline release from the renal sympathetic nerve endings in addition to its effect in the anterior hypothalamus and rostral ventrolateral medulla (RVLM) [1,2]. At RVLM neurons, Ang II acts either postsynaptically, by decreasing K
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