Figure 4 Differential protective effects of hydration and volume expansion according to administration route and fluid use Figure 4 | Differential protective effects of hydration and volume expansion according to administration route and fluid use. a | Oral water ingestion decreases osmolality and increases blood volume, which promptly suppresses vasopressin release from the pituitary gland123. Hypothalamic and hepatic osmoreceptors sense osmolality. Vagal afferences project the signals from hepatic osmoreceptors and cardiac volume receptors to the hypothalamus, which accelerate vasopressin suppression. The latter reduces water reabsorption in the collecting ducts, thus eliciting diuresis123. b | Isotonic saline, given orally or intravenously, does not change blood osmolality. Thus, no rapid osmoreceptor response occurs (which is the major reason behind the delayed response to saline). Saline loading increases the excretion of both water and sodium. As vasopressin controls tubular water reabsorption but not sodium reabsorption, it does not have an important role in the response to saline loading. Saline loading suppresses the renin–angiotensin–aldosterone system124, which relies, in part, on the signals of the atrial volume receptors. Low levels of angiotensin II increase renal sodium and water excretion by its direct effects on tubular reabsorption. Low aldosterone levels help to promote sodium excretion, but aldosterone effects are considerably delayed. Fähling, M. et al. (2017) Understanding and preventing contrast-induced acute kidney injury Nat. Rev. Nephrol. doi:10.1038/nrneph.2016.196