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

2021-05-06 10:51 AM

The ammonia (NH3) buffer excretes hydrogen ions in the manifold. Ammonia diffuses into the tube lumen, where it reacts with secreted H + to form NH4 +, which is then excreted.

Ammonia is the second buffering system in the renal tubule, even more, important than the phosphate buffering system. The buffer system consists of ammonia (NH3) and ammonium ions (NH4 +). Ammonium ions are synthesized from glutamine, which comes mainly from the metabolism of amino acids in the liver. Glutamine to the kidney is transported to the epithelial cells of the proximal tubule, which gradually increases as it passes through the Henle loop and distal tubule. Inside the cell, each molecule of glutamine is metabolized by a series of reactions to ultimately form 2 NH4 + and 2 HCO3-. The NH4 + ions are excreted into the lumen by a co-transport mechanism with sodium, which is reabsorbed. The HCO3- ions are transported across the membrane, along with Na + reabsorption into the interstitial fluid and transported by the glomerular capillaries. Each glutamine molecule metabolized in the proximal tube produces 2 NH4 + which are excreted in the urine and 2 HCO3- reabsorbed into the bloodstream.

Figure. NH4 + production and secretion in proximal tubular cells. Glutamine is metabolized in cells, producing NH4 + and bicarbonate. NH4 + is excreted into the renal tubules thanks to the co-transport of Na. For each metabolized glutamine, 2 NH4 + is created and 2 HCO3- released into the bloodstream.

Figure. The ammonia (NH3) buffer excretes hydrogen ions in the manifold. Ammonia diffuses into the tube lumen, where it reacts with secreted H + to form NH4 +, which is then excreted. For each NH4 + excreted, a new HCO3− is formed in the tubular cell and returned to the bloodstream.

In the manifold, NH4 + supplementation occurs through a different mechanism. Below, H + is secreted by the cell membrane into the lumen, where it combines with NH3 to form NH4 +, which is then excreted out. NH3 permeates the cells of the manifold, which can easily pass through the cell membrane in the lumen. However, this membrane is more or less permissive for NH4 +. So, once H + reacted with NH3 to form NH4 +, these NH4 + were trapped in the lumen and excreted in the urine. For each NH4 + excreted, a new HCO3 А is created and added to the bloodstream.

Chronic acidosis causes increased secretion of NH4 +. One of the most important functions of an ammonia buffering system is that it is under physiological control. An increase in H + stimulates glutamine metabolism in the kidney thereby increasing the formation of new NH4 + and HCO3-, whereas a decrease in H + inhibits glutamine metabolism in the kidney, reducing the formation of NH4 + and new HCO3-.

Under normal conditions, the amount of H + excreted by the ammonia buffer is about 50% of the acid excreted and 50% of the new HCO3 А produced by the kidneys. However, in chronic acidosis, the rate of NH4 + excretion can be increased to as much as 500 mEq/day. Therefore, with chronic acidosis, the mechanism by which acid is eliminated is NH4 + excretion. This process also provides the most important mechanism for generating new HCO3 А in chronic acidosis.

 

MOST VIEW

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

Prothrombin activation: initiates blood clotting

Estimated renal plasma flow: PAH clearance

Graphical analysis of high-volume heart failure

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

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

Red blood cells: differentiation and synthesis

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

Origin of lymphocytes: the body's resistance to infection

Pathophysiology of fever

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

The endocrine regulates tubular reabsorption

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

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