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30.4 : Regulation of Water Intake

Osmolality refers to the number of solute particles per kilogram of solvent in a solution. Plasma osmolality specifically indicates the total number of solute particles per kilogram of water in blood plasma. This value reflects the body's hydration status and is tightly regulated through mechanisms controlling water intake and output. While water consumption is a conscious decision, the body has intrinsic regulatory systems to maintain fluid balance. Dehydration, a state of water deficit leading to inadequate water supply in the blood and tissues, provides a clear example of these mechanisms at work.

Water loss occurs through breath, sweat, or urine and is primarily drawn from blood plasma. As blood solute concentration increases, the body activates the thirst response, a series of physiological events designed to restore balance. Osmoreceptors in the hypothalamus monitor plasma osmolality. When osmolality exceeds optimal levels, these receptors stimulate the thirst center in the hypothalamus, triggering the sensation of thirst and promoting water consumption.

The hypothalamus also releases antidiuretic hormone (ADH) via the posterior pituitary gland in response to increased plasma osmolality or significant volume depletion. ADH signals the kidneys to increase water reabsorption in the collecting ducts. Additionally, the hypothalamus sends signals to the salivary glands via the sympathetic nervous system, reducing watery (serous) saliva production due to decreased water availability and increasing mucus production. This leads to a dry mouth, further reinforcing the sensation of thirst.

A decrease in blood volume caused by water loss activates additional physiological responses. Baroreceptors in the aortic arch and carotid arteries detect reduced blood pressure due to the decreased blood volume. These sensors stimulate the heart to increase its rate and contraction strength to maintain blood pressure. Concurrently, the renin-angiotensin-aldosterone system (RAAS) in the kidneys is activated in response to decreased renal perfusion, sympathetic stimulation, or reduced sodium delivery to the distal tubule. Renin release leads to the production of angiotensin II, which stimulates thirst and prompts the adrenal glands to secrete aldosterone. Aldosterone increases sodium reabsorption in the distal tubules of the nephrons. Water follows sodium back into the bloodstream, provided antidiuretic hormone (ADH) is present to increase water permeability in the renal tubules.

Failure to consume adequate fluids results in dehydration, impairing the body's ability to function properly. Individuals with frequent vomiting or diarrhea are at higher risk of dehydration, as are infants, due to their lower body mass, which makes them more vulnerable to rapid fluid loss. Long-distance endurance athletes often experience dehydration during extended races, particularly if they do not replenish fluids effectively. Severe dehydration constitutes a medical emergency and can result in loss of consciousness, coma, or death if rehydration is not promptly administered.

From Chapter 30:

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30.4 : Regulation of Water Intake

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30.2 : Composition of Body Fluids

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30.6 : Disorder of Water Balance

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30.8 : Roles of Electrolytes: Chloride and Bicarbonate

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30.9 : Roles of Electrolytes: Calcium and Phosphate

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30.10 : Regulation of Sodium and Potassium

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30.11 : Acid-Base Balance

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30.12 : Buffer Systems in the Body

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30.13 : Protein Buffers in Blood Plasma and Cells

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30.15 : Bicarbonate-Carbonic Acid Buffer

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