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. Author manuscript; available in PMC: 2012 Jun 8.
Published in final edited form as: Cell Metab. 2011 Jun 8;13(6):619–620. doi: 10.1016/j.cmet.2011.05.007

Figure 1. Interactions between the brain and kidney in hypertension.

Figure 1

Mu and colleagues (Mu et al., 2011) show that sympathetic nerve activity, acting through β adrenergic receptors (βAR), in cooperation with glucocorticoid receptors (GR), suppresses WNK4 abundance and activates the sodium chloride cotransporter (NCC) to raise arterial pressure. The inset shows the distal nephron, with distal convoluted tubule (DCT, segments 1 & 2) and connecting tubules (CNT) expressing the NCC, the epithelial Na channel (ENaC), mineralocorticoid receptors (MR) and 11 beta-hydroxysteroid dehydrogenase 2 (11 β-HSD). Note the gradation of 11 β-HSD abundance, conferring steroid specificity.