The degree of concentration of the urine is regulated by ADH which controls the water permeability of the duct. It does so by causing additional water channels (aquaporins) in the lumen to be added to the duct to increase its permeability to water. It also increases the permeability of the collecting duct to urea, which then increases interstitial osmolarity in the medullary region. The volume of the filtrate in the collecting duct is reduced, so the volume decreases. The osmotic gradient in the medullary collecting duct concentrates the urine by drawing water from the filtrate as it travels through the medullary collecting duct. .
Also, according to our text " the adrenal cortex receives two opposing signals. One says, "Secrete aldosterone." The other says, "Do not secrete aldosterone." The rule of thumb that fluid balance integrating centers use when faced with conflicting signals is: Attempt to restore osmolarity to normal before restoring volume. The body has multiple mechanisms to deal with diminished blood volume, but high osmolarity causes cells to shrink and presents a more immediate threat to well-being. Thus, faced with decreased volume and increased osmolarity, the adrenal cortex will not secrete aldosterone" (Silverthorn 642). "Dehydration conditions can increase the concentration of urine to 1200mOsm" (Silverthorn 604), " then the NaCl will be excreted in a volume of 0.25L" (Silverthorne 630). According to my graph, my urine volume at its lowest was 0.3ml/min during the lag period. It was also very high in NaCl concentration which would indicate that the aldosterone was inhibited during dehydration in my case; however, with the increase in urine output (up to 5.7ml/min), the NaCl concentration levels also came down which was indicative of the resuming of aldosterone secretion to reabsorb the sodium and the decrease of ADH secretion to absorb water because sodium and water are reabsorbed together in exchange for hydrogen ions which reduced the pH of my urine as the output increased.
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