The endocrine regulates tubular reabsorption

2021-05-03 11:15 PM

To keep the volume of body fluids and solute concentrations at a constant level requires the kidneys to excrete different degrees of water and solutes, one independent of the other.

Because of the importance of maintaining an accurate balance between glomerular filtration and tubular reabsorption, many nerves, hormones and local mechanisms are involved in the regulation of reuptake. absorption of the renal tubules as well as glomerular filtration. The most striking importance of reabsorption is that the reabsorption of some substances can occur independently of others, especially in the presence of hormones.

To keep the volume of body fluids and solute concentrations at a constant level requires the kidneys to excrete different degrees of water and solutes, one independent of the other. For example, when potassium is absorbed, the kidneys will have to excrete more potassium than usual while maintaining the excretion of sodium and other electrolytes. Similarly, when sodium absorption changes, the kidneys change the amount of sodium excretion without having a major effect on other electrolytes. A summary of the important hormones involved in regulating renal tubular reabsorption, the tubular segments they work mainly, and their effects on water and electrolytes.


Board. Hormones regulate renal tubular reabsorption

Aldosterone increases sodium reabsorption increases potassium excretion

Aldosterone, secreted by cells in the adrenal cortex, plays an important role in regulating sodium reabsorption and excretion of potassium. Tubular cells subject to aldosterone are the principal cells of the cortical collecting tubule. The mechanism of action of aldosterone is through stimulation of the Na-K-ATPase pump in the basal membrane of the tubule segmental cell. Aldosterone also increases the permeability of sodium to the renal tubular lumen membrane.

The most important factors stimulating aldosterone secretion are (1) the potassium plasma concentration and (2) an increase in the concentration of angiotensin II, a substance closely related to sodium and a decrease in circulating volume or low blood pressure. Increased aldosterone excretion is closely related to the above situation, causing salt and water retention, increasing extracellularly, raising blood pressure back to normal levels.

The absence of aldosterone, as in the case of destruction of the adrenal gland structure or function (Addison's disease) causes significant sodium loss and potassium retention.

In contrast, an excess of aldosterone, as in the case of adrenal adenoma (Conn syndrome), is often associated with sodium retention and decreased potassium levels in part due to increased renal excretion of potassium. Sodium-ion regulation can be maintained in equilibrium even with low aldosterone concentrations, but potassium concentrations cannot be kept constant when aldosterone concentrations are low. Therefore, aldosterone plays an important role in regulating the concentration of potassium in the blood rather than the concentration of sodium.

Angiotensin II increases the reabsorption of sodium and water

Angiotensin II is probably the most powerful hormone to aid sodium reabsorption, Angiotensin II is formed closely related to hypotension and/or low extracellular fluid volume, as in the case of haemorrhage or excessive salt loss. sodium and water during severe diarrhoea or heavy sweating. Increasing levels of Angiotensin II help restore blood pressure and extracellular fluid to normal levels by increasing the renal tubular water and salt reabsorption through the following 3 mechanisms:

1. Angiotensin II increases the excretion of aldosterone, which increases sodium reabsorption.

2. Angiotensin II constricts the incoming arterioles, this will cause 2 effects on the hemodynamic of the capillaries around the renal tubules, resulting in an increase in sodium and water reabsorption. The first effect is, the constriction of the arterioles reduces the hydrostatic pressure in the capillary lumen, increases the pressure of reabsorption, which is evident in the proximal tubule. Second, the incoming arterioles, by reducing renal blood flow, will increase the glomerular filtration fraction, increase the protein concentration as well as the colloid pressure in the capillaries around the renal tubules; This mechanism increases the pressure of reabsorption, increases water and sodium salt retention.

3. Angiotensin II directly increases Na-tri reabsorption in the proximal tubule, the distal tubule, the distal tubule and the manifold. One of these direct mechanisms of action is that Angiotensin II stimulates the Na-K-ATPase pump in the basal membrane of the tubular cells. The second mechanism is to stimulate the Na-H pump in the lumen of the renal tubule, especially the proximal tubule. The third mechanism of Angiotensin II is to stimulate the Na-HCO3 co-transport channel in the basal membrane of the cell.


Figure. The direct action of Angiotensin (Ang II) increases sodium reabsorption in the proximal tubule. Ang II stimulates Na-H (NHE) exchange in the lumen and Na-K-ATPase channel as well as Na-HCO3 co-transport in the basal membrane.

These mechanisms also occur in many sections of the kidney, including the spinning of the Henle, the distal tubule and the manifold.

Consequently, Angiotensin II stimulates sodium transport channels on both sides of the cell membrane in most sections of the renal tubule. This makes angiotensin an important role in the retention of salt and water, allowing us to use salt in large variations without affecting extracellular fluid volume or blood pressure.

At the same time Angiotensin increases the reabsorption of salt and water, the vasoconstriction of the incoming arterioles also helps maintain the excretion of excess products of metabolic processes such as urea, creatinine, which are naturally excreted mainly due to glomerular filtration rate. Therefore, increasing angiotensin II allows the kidneys to retain salt and water without affecting the excretion of metabolic products.

ADH increases water reabsorption

The most important mechanism of ADH is to increase the permeability of the membrane of the distal tubule to water, the collecting duct and the papillary canal. This mechanism helps the body to retain water in circulation, especially in case of dehydration. In the face of ADH, the permeability of the distal tubule and the tubule to water is very low, that is, the kidneys excrete a large volume of urine, a condition called diabetes inspidus. Therefore, ADH plays a role in determining the degree of urine dilution or concentration.

ADH specifically binds to the V2 receptor present in the distal tubule, the manifold and the papillary canal, increases cAMP synthesis and activates the protein kinase.

This activation causes an intracellular protein, Aquapor-in 2 (AQP-2), to migrate to the cell membrane in the lumen. The AQP-2 molecule binds together and fuses with the cell membrane to form water channels that allow the rapid diffusion of water across the cell membrane.

In addition to AQP-2, there are also AQP-3, AQP-4 in the basal membrane that allows water to exit the cell into the interstitial space rapidly, although this has not been shown to be due to its role. ADH.

Chronic elevation of ADH also increases AQP-2 synthesis through transcription of the gene encoding AQP2. When the ADH concentration is low, the AQP-2 molecules return to the cytoplasm, the permeability of the membrane to water decreases. The effects of ADH on cytology are discussed in Chapter 76.


Figure. Mechanism of action of arginine vasopressin (AVP) on epithelial cells of the distal tubule, the manifold and the papillary canal. AVP binds to V2 receptors, stimulates protein G, activates adenylate cyclase (AC), increases cyclic AMP synthesis (cAMP). This substance, activating the protein kinase A and the intracellular protein phosphorylation, moves aquaporin-2 (AQP-2) onto the lumen membrane. AQP-2 molecule fuses the membrane to form a water channel. On the basal membrane side, AQP-3 and AQP-4 allow water to exit the cell into the intercellular space, although there are no studies showing that these aquaporins are influenced by AVP.

Atrial Natriuretic Peptide reduces the reabsorption of sodium and water

When specific atrial cells stretch as plasma volume increases and atrial pressure increases, they secrete a peptide called atrial diuretic sodium peptide (ANP). Increased levels of this peptide in turn inhibit the renal tubular reabsorption of sodium and water, especially in the collecting tubules. ANP also inhibits renin secretion and thus angiotensin II formation, thereby reducing tubular reabsorption. This reduced sodium and water reabsorption increases urinary excretion, helping to return blood levels to normal.

An increased concentration of ANP in congestive heart failure occurs when the atrium is strained because the ventricles have decreased pumping. Increased ANP helps reduce sodium and water retention in heart failure.

Parathyroid hormone increases calcium reabsorption

Parathyroid hormone is one of the most important calcium-regulating hormones in the body. Its primary effect in the kidney is to increase renal tubular calcium reabsorption, especially in the distal tubules and perhaps even the loops of Henle. Parathyroid hormone also has other effects, including inhibition of phosphates reabsorption in the proximal tubule and stimulation of magnesium reabsorption via the Henle loop.



Pathophysiology of cardiogenic shock

Urine formation: Reabsorbed glomerular filtration

Air in and out of the lungs: pressure causes the movement of air

Mechanism of urine concentration: osmotic pressure changes in different segments of the renal tubule

Absorption and excretion of potassium through the kidneys

Nephron: The functional unit of the kidney

Estimated renal plasma flow: PAH clearance

Prothrombin activation: initiates blood clotting

Pulmonary capillary dynamics: capillary fluid exchange and pulmonary interstitial fluid dynamics

Graphical analysis of high-volume heart failure

Red blood cells: differentiation and synthesis

Calculate the glomerular filtration rate (GFR): the forces that cause the filtration process

Ammonia buffering system: excretes excess H + and creates new HCO3

Concentrated urine formation: urea contributes to increased osmotic pressure in the renal medullary

Reduced sodium chloride, dilates arterioles, increases Renin release.

Extracellular fluid distribution between interstitial space and blood vessels

The proximal tubule reabsorption: active and passive reabsorption

Pathophysiology of fever

Origin of lymphocytes: the body's resistance to infection

Acidosis causes a decrease in HCO3- / H + in renal tubular fluid: compensation mechanism of the kidney

Sodium channel blockers: decrease the reabsorption of sodium in the manifold

Self-regulation of glomerular filtration rate and renal blood flow

Physiological anatomy of the kidneys and urinary system

The myogenic mechanism itself regulates renal blood flow and glomerular filtration rate

The kidneys excrete sodium and fluid: feedback regulates body fluids and arterial pressure