Antidiuretic hormone measurement

Water Deficiency. This condition occurs when water output exceeds intake. Water is continually losl by way of the lungs, skin, and kidneys and dius a deficiency of body water will occur if a critical minimal supply is not maintained. Decreased intake when water is available is uncommon. Very rarely, a brain malfunction may interfere with one s sense of diirst. Increased output of water can result from many causes. For example, a person with diabetes insipidus who lacks ADH (antidiuretic hormone) or a person whose kidneys do not respond normally to ADH, as in instances of nephrogenic diabetes insipidus, will increase water output Other diseases which may cause excess excretion of water include osmotic diuresis, hypercalcemia, hypokalemia, chronic pyelonephritis, and sickle cell anemia, among others. Excessive water losses are also experienced in some cases with advanced age and in some burn cases. Two clinical features are good measures of dehydration—weight loss of the patient and an elevation of the serum sodium concentration. In situations of dehydration, the body initiates mechanisms which manipulate the transfer of water from one compartment to the next, retaining water in those cells and organs where it is most needed. 

Another 3D model had been developed with immortalized human renal cortical cells embedded into a mix of Matrigel and rat tail collagen (DesRochers et al., 2013). These cells displayed some features of PTC but performed also functions that are not typical for PTC. For instance, the cells were responsive to antidiuretic hormone, whereas they did not respond to parathyroid hormone. The effects of cisplatin, gentamicin, and doxorubicin were tested by measuring cell viability, LDH release, and increase of KIM-1 and NGAL. In compatison to 2D cultures, the 3D model did not clearly improve the results. Also here positive responses to doxorubicin were observed, and in this case the 3D model was more sensitive than 2D cultures to this usually non-PT-damaging drag. 

A very interesting analytical approach was chosen by Updike and Treichel [286] who constructed a tissue sensor for antidiuretic hormone (ADH) using a toad bladder tissue membrane over the surface of a sodium ion-sensing glass electrode. The measurement was based on the enhancement of sodium ion transport in the presence of ADH. The bladder membrane must be oriented with its mucosal side towards the sodium electrode because the transport occurs only from the mucosal to the serosal side. The ADH assay was very fast (response time about 10s) however, sodium transport was also affected by some other hormones and thus this method is not specific. 

There are two components to the regulation of ECE sodium the total amount of sodium retained and its concentration. The former is regulated by mechanisms that directly affect sodium, whereas the latter is essentially regulated via water balance. Thus, whatever sodium is retained in ECF is clothed with the appropriate amount of water to maintain the normal plasma sodium concentration within narrow limits deviations of less than 1% (hard to measure in the laboratory) trigger corrective responses. Thus, a raised plasma sodium concentration (e.g., after water loss) stimulates both thirst and renal water conservation antidiuretic hormone (ADH) from the posterior pituitary reduces urine output through its effect on the renal collecting ducts. Even one of these mechanisms can defend body water thus diabetes insipidus (inadequate production or effect of ADH) does not cause severe dehydration but polydipsia (increased fluid intake thirst is a sensation). 

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