Plasma osmolarity

Blood pressure and electrolyte composition by regulating mechanisms involved with urine output, thirst, salt appetite, maintenance of plasma osmolarity, and vascular smooth muscle tone... 

Antidiuretic hormone promotes the reabsorption of water from the tubules of the kidney, or antidiuresis. Specifically, it acts on the collecting ducts and increases the number of water channels, which increases the diffusion coefficient for water. This results in the body s conservation of water and the production of a low volume of concentrated urine. The reabsorbed water affects plasma osmolarity and blood volume. This effect of ADH on the kidney occurs at relatively low concentrations. At higher concentrations, ADH causes constriction of arterioles, which serves to increase blood pressure. Antidiuretic hormone secretion is regulated by several factors ... 

The primary factor that influences ADH secretion is a change in plasma osmolarity. Osmoreceptors in the hypothalamus are located in close proximity to the ADH-producing neurosecretory cells. Stimulation of these osmoreceptors by an increase in plasma osmolarity results in stimulation of the neurosecretory cells an increase in the frequency of action potentials in these cells and the release of ADH from their axon terminals in the neurohypo-... 

Hypothalamic osmoreceptors have a threshold of 280 mOsM. Below this value, they are not stimulated and little or no ADH is secreted. Maximal ADH levels occur when plasma osmolarity is about 295 mOsM. Within this range, the regulatory system is very sensitive, with measurable increases in ADH secretion occurring in response to a 1% change in plasma osmolarity. Regulation of ADH secretion is an important mechanism by which a normal plasma osmolarity of 290 mOsM is maintained. 

Vasopressin (antidiuretic hormone) is a peptide synthesized in the hypothalamus and secreted from the neurohypophysis of the pituitary gland. This substance plays an important role in the long-term regulation of blood pressure through its action on the kidney to increase reabsorption of water. The major stimulus for release of vasopressin is an increase in plasma osmolarity. The resulting reabsorption of water dilutes the plasma toward its normal value of 290 mOsM. This activity is discussed in more detail in Chapter 10 (the endocrine system) and Chapter 19 (the renal system). 

The kidneys also regulate the osmolarity of extracellular fluid, in particular plasma osmolarity. The maintenance of plasma osmolarity close to 290 mOsm prevents any unwanted movement of fluid into or out of the body s cells. An increase in plasma osmolarity causes water to leave the cells, leading to cellular dehydration a decrease in plasma osmolarity causes water to enter the cells, leading to cellular swelling and possibly lysis. Plasma osmolarity is regulated primarily by altering the excretion of water in the urine. 

The maintenance of plasma volume and plasma osmolarity occurs through regulation of the renal excretion of sodium, chloride, and water. Each of these substances is freely filtered from the glomerulus and reabsorbed from the tubule none is secreted. Because salt and water intake in the diet may vary widely, the renal excretion of these substances is also highly variable. In other words, the kidneys must be able to produce a wide range of urine concentrations and urine volumes. The most dilute urine produced by humans is 65 to 70 mOsm/1 and the most concentrated the urine can be is 1200 mOsm/1 (recall that the plasma osmolarity is 290 mOsm/1). The volume of urine produced per day depends largely upon fluid intake. As fluid intake increases, urine output increases to excrete the excess water. Conversely, as fluid intake decreases or as an individual becomes dehydrated, urine output decreases in order to conserve water. 

Recall that reabsorption of water is important in the regulation of plasma osmolarity. As the levels of ADH increase and more water is reabsorbed from the kidneys, the plasma is diluted and plasma osmolarity decreases. Conversely, as the levels of ADH decrease and more water is lost in the urine, plasma becomes more concentrated and plasma osmolarity increases. Factors involved in the release of ADH are discussed further in subsequent sections. 

Production of urine of varying concentrations. In order to regulate plasma volume and osmolarity effectively, the kidneys must be able to alter the volume and concentration of the urine that is eliminated. Accordingly, the concentration of urine may be varied over a very wide range depending upon the body s level of hydration. The most dilute urine produced by the kidneys is 65 to 70 mOsm/1 (when the body is overhydrated) and the most concentrated urine is 1200 mOsm/1 (when the body is dehydrated). (Recall that plasma osmolarity is 290 to 300 mOsm/1.)... 

Diuretics are drugs that cause an increase in urine output. It is important to note that, except for the osmotic diuretics, these drugs typically enhance the excretion of solute and water. Therefore, the net effect of most diuretics is to decrease plasma volume, but cause little change in plasma osmolarity. Five classes of diuretics and their major sites of action are ... 

Control of water excretion regulation of plasma osmolarity... 

The osmoreceptors of the hypothalamus monitor the osmolarity of extracellular fluid. These receptors are stimulated primarily by an increase in plasma osmolarity they then provide excitatory inputs to the thirst center and the ADH-secreting cells in the hypothalamus. The stimulation of the thirst center leads to increased fluid intake. The stimulation of the ADH-secreting cells leads to release of ADH from the neurohypophysis and, ultimately, an increase in reabsorption of water from the kidneys and a decrease in urine output. These effects increase the water content of the body and dilute the plasma back toward normal. Plasma osmolarity is the major stimulus for thirst and ADH secretion two additional stimuli include ... 

The single most important effect of anti-diuretic hormone is to conserve body water, by reducing the loss of water in urine. In the absence of anti-diuretic hormone, the collecting ducts of the kidney are virtually impermeable to water. Anti-diuretic hormone stimulates water re-absorbtion through the insertion of water channels , or aquaporins (see Section 10.5), into the membranes of kidney tubules. Aquaporins transport solute-free water through tubular cells and back into blood, leading to a decrease in plasma osmolarity and an increased osmolarity of urine. 

Regulation of anti-diuretic hormone secretion is primarily through the plasma osmolarity. Osmolarity is sensed in the hypothalamus by neurons known as osmoreceptors, which in turn stimulate secretion from those neurons that produce anti-diuretic hormone. Secretion of antidiuretic hormone is also simulated by decreases in blood pressure and volume, conditions sensed by stretch receptors in the heart and large arteries. Changes in blood pressure and volume are not nearly as sensitive a stimulator as increased osmolarity, but are nonetheless potent in severe conditions. For example, loss of 15-20% of blood volume by haemorrhage results in a massive secretion of anti-diuretic hormone. Another potent stimulus of anti-diuretic hormone is nausea and vomiting, both of which are controlled by regions in the brain with links to the hypothalamus. 

Hyperosmotemia Increase in the plasma osmolar (salt) concentra-... 

Vasopressin promotes increased resorption of water in the renal distal tubule by stimulating insertion of water channels or aquaporins into the apical membranes of kidney tubules. Water is resorbed across the renal epithelium into the blood leading to a decrease in plasma osmolarity and an increase in the osmolarity of urine. In DI, this process is impaired, leading to excessive urine production, hi the absence of vasopressin, the kidney cannot resorb water and it flows out as urine. This condition can arise from a deficiency in vasopressin secretion from the posterior pituitary as a result of hypothalamic tumors, injury (as in the case of this patient) or infection. Alternately,... 

Sharp drc in plasma osmolarity in carp, Cyprinus carpio... 

Ruid is drawn from the cells to decrease plasma osmolarity. 

Each point is the mean of 2 pigs. The shaded area on the lower graph (b) is the limits of plasma osmolarity. t = dosing started. I = dosing stopped. 

For the chamber, see Rehm WS, Dennis WH, Schlesinger H. Electrical resistance of the mammalian stomach. Am J Physiol 181 451-470, 1955. For attempts to modify the blood, see Thull NB, Rehm WS. Composition and osmolarity of gastric juice as a function of plasma osmolarity. Am J Physiol 185 317-324,1956. For early isolated mucosa work, see Rehn WS. Acid secretion, resistance, short-circuit current and voltage clamping in frog s stomach. Am J Physiol 203 63-72, 1962. 

Hyperglycaemic coma develops in people with insulin-dependent diabetes because, despite an abnormally high plasma concentration of glucose, tissues are unable to utilize it in the absence of insulin. The high plasma concentration of glucose leads to elevated plasma osmolarity, which results in coma. In such cases insulin injection is required. 

Osmotic and diffusive processes, which occur in tissue or blood treated by chemical agents, are important for the efficiency, fastness and reversibility of optical clearing. For blood the index mismatch between erythrocyte cytoplasm and blood plasma is essential, however, erythrocyte volume and shape defined by blood plasma osmolarity and aggregation capability are also important [84, 85]. Recently the... 

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