Key result
The subfornical organ plays a critical role in mediating fluid intake responses to dehydration and central angiotensin II.
This review summarizes the physiological mechanisms by which the brain renin-angiotensin system and the subfornical organ regulate fluid intake and blood pressure in response to dehydration.
May guide research on central thirst mechanisms; leaves open clinical translation to fluid disorders or hypertension.
It is critical for cells to maintain a homeostatic balance of water and electrolytes because disturbances can disrupt cellular function, which can lead to profound effects on the physiology of an organism. Dehydration can be classified as either intra- or extracellular, and different mechanisms have developed to restore homeostasis in response to each. Whereas the renin-angiotensin system (RAS) is important for restoring homeostasis after dehydration, the pathways mediating the responses to intra- and extracellular dehydration may differ. Thirst responses mediated through the angiotensin type 1 receptor (AT1R) and angiotensin type 2 receptors (AT2R) respond to extracellular dehydration and intracellular dehydration, respectively. Intracellular signaling factors, such as protein kinase C (PKC), reactive oxygen species (ROS), and the mitogen-activated protein (MAP) kinase pathway, mediate the effects of central angiotensin II (ANG II). Experimental evidence also demonstrates the importance of the subfornical organ (SFO) in mediating some of the fluid intake effects of central ANG II. The purpose of this review is to highlight the importance of the SFO in mediating fluid intake responses to dehydration and ANG II.
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Coble et al. (2014) conducted a review in Dehydration. Subfornical organ (SFO) mediation was evaluated. The subfornical organ plays a critical role in mediating fluid intake responses to dehydration and central angiotensin II.
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