Approximately 180 liters of water are filtered through the glomeruli daily, of which roughly 1 per cent (2 liters) is normally excreted. Daily urine volume may vary from 400 ml to more than 15 liters, depending on water requirements. The kidneys strictly preserve plasma volume and osmolality within a limited range. Two-thirds of filtered water is isosmotically reabsorbed in the proximal tubule, largely dependent on sodium reabsorption. The remaining water reabsorption along the nephron is contingent on the interaction of renal interstitium osmolality, tubule water permeability, and ADH levels. ADH, which is produced in the hypothalamus, plays a crucial role in regulating plasma osmolality by increasing water reabsorption along the distal convoluted tubule and collecting ducts. Hypothalamic osmoreceptors sense deviations in plasma tonicity (changes of 1 per cent), enhancing and inhibiting ADH output with increased and decreased urine osmolality respectively. Large disturbances in extracellular fluid volume (10 per cent) also modify ADH secretion via baroreceptor mediators, sometimes overruling the regulation by tonicity; for example, increased ADH complicates and exacerbates hyponatremia associated with volume depletion or cardiac failure. Catecholamines, angiotensin II, prostaglandins, and nicotine may stimulate ADH secretion via baroreceptor activation. Other non-osmotic stimuli of ADH release are nausea, pain, anxiety, drugs, hypothyroidism, hypopituitarism, and pulmonary and cerebral disorders. Isoproterenol (isoprenaline) increases ADH release (by stimulating b-adrenergic receptors), while it is indirectly suppressed by the vasopressor norepinephrine (noradrenaline), dopamine antagonists such as haloperidol and promethazine (which inhibit the emetic center), and ethanol. Abnormal ADH release may also occur in tumors; the syndrome of inappropriate release of ADH is a difficult diagnosis since it requires the exclusion of all the causes mentioned above for non-osmotic ADH release.
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