However, it is not the only sugar that can produce a diuretic effect. In cases of poorly controlled diabetes mellitus, glucose levels exceed the capacity of the tubular glucose symporters, resulting in glucose in the urine.
The unrecovered glucose becomes a powerful osmotic diuretic. Classically, in the days before glucose could be detected in the blood and urine, clinicians identified diabetes mellitus by the three Ps: polyuria diuresis , polydipsia increased thirst , and polyphagia increased hunger. Another hormone responsible for maintaining electrolyte concentrations in extracellular fluids is aldosterone , a steroid hormone that is produced by the adrenal cortex. In contrast to ADH, which promotes the reabsorption of water to maintain proper water balance, aldosterone maintains proper water balance by enhancing Na reabsorption and K secretion from extracellular fluid of the cells in kidney tubules.
Because it is produced in the cortex of the adrenal gland and affects the concentrations of minerals Na and K , aldosterone is referred to as a mineralocorticoid , a corticosteroid that affects ion and water balance. Aldosterone release is stimulated by a decrease in blood sodium levels, blood volume, or blood pressure, or an increase in blood potassium levels. It also prevents the loss of Na from sweat, saliva, and gastric juice. The reabsorption of Na also results in the osmotic reabsorption of water, which alters blood volume and blood pressure.
Aldosterone production can be stimulated by low blood pressure, which triggers a sequence of chemical release, as illustrated in Figure 1. When blood pressure drops, the renin-angiotensin-aldosterone system RAAS is activated. Cells in the juxtaglomerular apparatus, which regulates the functions of the nephrons of the kidney, detect this and release renin.
Renin, an enzyme, circulates in the blood and reacts with a plasma protein produced by the liver called angiotensinogen.
When angiotensinogen is cleaved by renin, it produces angiotensin I, which is then converted into angiotensin II in the lungs. Angiotensin II functions as a hormone and then causes the release of the hormone aldosterone by the adrenal cortex, resulting in increased Na reabsorption, water retention, and an increase in blood pressure. Angiotensin II in addition to being a potent vasoconstrictor also causes an increase in ADH and increased thirst, both of which help to raise blood pressure.
This condition can arise from either of two situations:. The major sign of either type of diabetes insipidus is excessive urine production. Some human patients produce as much as 16 liters of urine per day! If adequate water is available for consumption, the disease is rarely life-threatening, but withholding water can be very dangerous. Hypothalamic diabetes insipidus can be treated with exogenous antidiuretic hormone. Luteinizing Hormone and Follicle-stimulating Hormone.
Updated Send comments to Richard. Bowen colostate. A Finnish translation of this page by Elsa Jansson is available at Finnish translation.
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ADH is a hormone secreted from the posterior pituitary gland in response to increased plasma osmolarity i. The increased plasma osmolarity is sensed by osmoreceptors in the hypothalamus, which will stimulate the posterior pituitary gland to release ADH.
ADH will then act on the nephrons of the kidneys to cause a decrease in plasma osmolarity and an increase in urine osmolarity. ADH increases the permeability to water of the distal convoluted tubule and collecting duct, which are normally impermeable to water. This effect causes increased water reabsorption and retention and decreases the volume of urine produced relative to its ion content. After ADH acts on the nephron to decrease plasma osmolarity and leads to increased blood volume and increase urine osmolarity, the osmoreceptors in the hypothalamus will inactivate, and ADH secretion will end.
Due to this response, ADH secretion is considered to be a form of negative feedback.
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