Control of osmotic pressure and sodium concentration: ADH and thirst mechanism

2021-05-05 09:48 AM

In the absence of ADH-thirst mechanisms, there are no other feedback mechanisms capable of adequately regulating plasma sodium concentrations and osmotic pressure.

In a healthy person, the osmoreceptor-ADH and thirst mechanisms work in tandem to precisely regulate extracellular fluid osmolality and sodium concentration, despite the constant challenges of loss. country. Even with additional challenges, such as high salt intake, these feedback systems are capable of keeping a reasonably consistent plasma osmolality. The figure shows that an increase in sodium intake as high as 6 times normal has only a minor effect on plasma sodium concentrations while both the ADH and thirst mechanisms are functioning normally.

Figure. Effects of large changes in sodium intake on extracellular sodium concentrations in dogs under normal conditions (red line) and after the thirst response system and antidiuretic hormone (ADH) system blocked (green line). Note that the control of sodium concentration in the extracellular fluid is poor in the absence of these feedback systems.

When either the ADH or the thirst mechanism is impaired, the other can normally control the extracellular osmotic pressure and sodium concentration with reasonable efficiency, provided adequate amounts are available. fluid in order to balance the required daily urine volume and dehydration caused by respiration, sweating, or gastrointestinal tract. However, if both ADH and thirst mechanisms fail simultaneously, then plasma sodium concentrations and osmotic pressure are difficult to control; therefore, when sodium intake increases after suppressing the entire ADH-thirsty system, relatively large changes in plasma sodium concentrations occur.

In the absence of ADH-thirst mechanisms, there are no other feedback mechanisms capable of adequately regulating plasma sodium concentrations and osmotic pressure.

The role of angiotensin II and aldosterone in controlling extracellular fluid osmolality and sodium concentration

Both angiotensin II and aldosterone play an important role in regulating sodium reabsorption by the renal tubules. When sodium intake is low, increasing concentrations of these hormones stimulate sodium reabsorption by the kidneys and thus prevent a large loss of sodium, although sodium intake can drop as low as 10% compared to normal. Conversely, with high sodium intakes, reducing the formation of these hormones allows the kidneys to excrete large amounts of sodium.

Figure. Effects of large changes in sodium intake on extracellular sodium concentrations in dogs under normal conditions (red line) and after aldosterone response is blocked (blue line). Note that sodium concentrations are maintained relatively constant over this large sodium range, with or without aldosterone response control.

Because of the importance of angiotensin II and aldosterone’s in regulating sodium excretion by the kidneys, one may erroneously infer that they also play an important role in regulating extracellular fluid sodium levels. Although these hormones increase the amount of sodium in the extracellular fluid, they also increase extracellular fluid volume by increasing water reabsorption along with sodium. Consequently, angiotensin II and aldosterone’s have little effect on sodium concentrations except under extreme conditions.

This relative unimportance of aldosterone in the regulation of the extracellular fluid sodium concentration is shown by the experiment in the figure. This figure shows the effect on the plasma sodium concentration of changes in sodium intake by more than six times under two conditions: (1) under normal conditions and (2) after the aldosterone feedback system is impaired. intercepted by removing the adrenal glands and infusing aldosterone animals at a constant rate so that plasma concentrations cannot be increased or decreased. Note that when sodium intake has increased sixfold, plasma concentrations change only about 1-2% in both cases. This finding suggests that even without a functional feedback system aldosterone, plasma sodium concentrations can be well regulated.

There are two main reasons why the changes of angiotensin II and aldosterone do not have a major effect on plasma sodium concentrations. First, as discussed earlier, angiotensin II and aldosterone increase both sodium reabsorption and water reabsorption by the renal tubules, leading to an increase in extracellular fluid volume and sodium quantity but with little change. sodium concentration. Second, as long as the ADH-thirst mechanism is functional, any propensity to increase plasma sodium concentrations is compensated for by increased water intake or increased plasma ADH excretion, that is. tends to return to normal in dilution of the extracellular fluid. The ADH-thirst system overshadows many angiotensin II and aldosterone systems in regulating sodium concentrations under normal conditions. Even in patients with primary hyperaldosteronism,

Under extreme conditions caused by complete loss of aldosterone secretion as a result of removal of the adrenal glands or in patients with Addison's disease (severely impaired excretion or total aldosterone deficiency), there is a tremendous loss of sodium through the kidneys, which can lead to a decrease in the concentration of sodium in the blood plasma. One of the reasons for this is that this large loss of sodium ultimately causes severe depletion of fluid volume and a decrease in blood pressure, which can trigger the thirst mechanism through cardiovascular reflexes. . This activation leads to a further dilution of the sodium concentration in the blood plasma, although an increase in water intake minimizes a decrease in body fluid volume under these conditions.

Hence, extreme situations exist in which plasma sodium concentrations can vary significantly, even with an ADH-thirsty functional mechanism. Despite this, the ADH-thirst mechanism is by far the most powerful feedback system in the body in controlling extracellular fluid osmolality and sodium concentration.

Salt craving mechanism in controlling extracellular fluid sodium concentration and extracellular fluid volume

Maintaining normal extracellular fluid volume and sodium concentration requires a balance between sodium excretion and sodium intake. In modern civilizations, sodium intake is almost always greater than is required for homeostasis. In fact, the average sodium intake for a person in industrialized cultures who eats processed foods is typically between 100 and 200 mEq/day, although humans can survive and function. is normal, while an entry is only 10 to 20 mEq/day. So most people eat too much sodium than is necessary for homeostasis, and evidence indicates that our regularly high sodium intake may contribute to cardiovascular disorders like high blood pressure. pressure.

Salt cravings are due in part to the fact that animals and humans love salt and eat it regardless of whether they are salt deficient or not. Salt cravings also have a regulating component that has a behavioural movement to capture salt when a sodium deficiency exists in the body. This behavioural movement is especially important in herbivores, which eat a low-sodium diet, but salt cravings may also be important in people with a severe sodium deficiency. such as occurring in Addison's disease. In this case, there is a deficiency in aldosterone secretion, which causes an excessive loss of sodium in the urine and leads to a decrease in extracellular fluid volume and a decrease in sodium concentration; even these changes evoke salt cravings.

In general, major stimuli to increase salt cravings are associated with sodium deficiency and a decrease in blood volume or a decrease in blood pressure associated with circulatory failure.

The neural mechanism for salt craving is similar to the mechanism of thirst. Several of the similar nerve centres in the AV3V region of the brain appear to be involved because damage in this area frequently affects both thirst and salt cravings simultaneously in animals. . In addition, the circulatory reflexes prompted by low blood pressure or a decrease in blood volume affect both thirst and salt cravings at the same time.

 

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