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. 2022 Apr 19;474(8):759–770. doi: 10.1007/s00424-022-02690-y

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© The Author(s) 2022

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 2 — Regulation of tissue pO₂ (p_tO₂) by neuro-hormonal agents. The vasoconstrictor factors that reduce RBF and O₂ delivery (DO₂) generally also stimulate sodium reabsorption (T_Na) and increase O₂ consumption (QO₂). Conversely, the vasodilator factors that increase RBF and DO₂ may also act to reduce T_Na and QO₂. However, these effects are blunted by two mechanisms: increasing RBF also raises GFR and therefore T_Na, whereas increases in T_Na in the proximal tubule and the ascending limb may reduce NaCl delivery to the macula densa and raise RBF via tubulo-glomerular feedback (TGF). Hence, the effectiveness of p_tO₂ regulation also depends on how neuro-hormonal agents modulate the coupling between RBF and GFR (i.e., by changing the filtration fraction), or between T_Na and QO₂ (i.e., by changing the metabolic efficiency of Na⁺ transport). These effects are not explicitly shown in the figure (see text). Not shown either are the synergistic and antagonistic effects between various neuro-hormonal agents