Abstract:
Water is critical for survival and thirst is a powerful way of ensuring that fluid levels remain in balance. Overconsumption, however, can have deleterious effects, therefore optimization requires a need to balance the drive for water with the satiation of that water drive. This review will highlight our current understanding of how thirst is both generated and quenched, with particular focus on the roles of angiotensin II, glucagon like-peptide 1, and estradiol in turning on and off the thirst drive. Our understanding of the roles these bioregulators play has benefited from modern behavioral analyses, which have improved the time resolution of intake measures, allowing for attention to the details of the patterns within a bout of intake. This has led to behavioral interpretation in ways that are helpful in understanding the many controls of water intake and has expanded our understanding beyond the dichotomy that something which increases water intake is simply a \"stimulator\" while something that decreases water intake is simply a \"satiety\" factor. Synthesizing the available information, we describe a framework in which thirst is driven directly by perturbations in fluid intake and indirectly modified by several bioregulators. This allows us to better highlight areas that are in need of additional attention to form a more comprehensive understanding of how the system transitions between states of thirst and satiety.
摘要:
水对于生存至关重要,口渴是确保液体水平保持平衡的有力方法。过度消费,然而,会产生有害影响,因此,优化需要平衡水驱动与满足水驱动。这篇评论将强调我们目前对口渴是如何产生和消除的理解,特别关注血管紧张素II的作用,胰高血糖素样肽1和雌二醇在打开和关闭口渴驱动中。我们对这些生物调节剂所扮演的角色的理解得益于现代行为分析,提高了进气措施的时间分辨率,允许在一次摄入中注意图案的细节。这导致了行为解释,有助于理解水的摄入的许多控制,并扩大了我们的理解,超越了二分法,即增加水摄入量的东西只是一个“刺激器”,而减少水摄入量的东西只是一个“饱腹感”因素。综合可用信息,我们描述了一个框架,其中口渴是由流体摄入的扰动直接驱动,并由几种生物调节剂间接改变。这使我们能够更好地突出需要额外关注的领域,以更全面地了解系统如何在口渴和饱腹状态之间过渡。