Renal interstitial fluid

If tubular reabsorption does not meet physiological requirements, a renal tubular mechanism for generating bicarbonate is called into play this mechanism is shown in outline in Figure 1.4B. Carbon dioxide from metabolism reacts with water to yield hydrogen ions, which are actively pumped into the tubular fluid rendering the urine acid, and bicarbonate ions, which diffuse into the renal interstitial fluid and hence into the general extracellular fluid of the body. The tubules continually add bicarbonate to the body by this mechanism. 

Figure 3j5. A. The movements of hydrogen and potassium ions between intra- and extracellular fluid compartments produced by a fall in hydrogen ion concentration of the extracellular fluid. B. Similarly for a fall in potassium ion concentration of the extracellular fluid. C. Movements of ions between the renal tubular fluid and the renal interstitial fluid sodium, chloride and bicarbonate are reabsorbed, hydrogen and potassium ions are secreted.

The total transfer of charge across the tubular wall must be zero if this were not so, a large electrical potential would rapidly develop and prevent further net movement of charge. For every Mole of sodium ions transferred from tubular fluid to the renal interstitial fluid, there must be an accompanying Mole of charge to balance this. Whilst most of this is matched by chloride, the movement of other ions must make good the disparity. As shown by the... 

For each hydrogen ion excreted, one bicarbonate ion is added to the intracellular fluid of the renal tubular cell. The intracellular concentration of bicarbonate rises. In Figure 7.1 B, the reaction of CO2 is omitted and only the products Fl and HCO, are reproduced from Figure 7.1 A. Bicarbonate, being charged, is insoluble in lipid and so diffuses extremely slowly across the lipid regions of the cell membrane. On the aspect of the tubular cell membrane facing the interstitial fluid, the lipid membrane is traversed by protein macromolecules which comprise a carrier mechanism for bicarbonate ions (section A.l). The rise in intracellular concentration of bicarbonate leads to transfer of bicarbonate from the renal tubular cell cytoplasm to the renal interstitial fluid. 

In the proximal tubule, the bicarbonate entering the renal interstitial fluid and thence being removed by the renal venous blood arises indirectly from filtered bicarbonate. In the distal lengths of the tubule, the hydrogen ions secreted into the urine stay there whilst the bicarbonate ions added from the renal tubular cell cytoplasm to the interstitial fluid are now new bicarbonate ions, not merely ions retrieved from the tubular fluid. 

A.1 The bicarbonate-sodium co-transporter for movement from the renai tubular intracellular fluid to the renal interstitial fluid... 

Neurons are very sensitive to changes in the pH of the interstitial fluid surrounding them. Normally, the pH of arterial blood is 7.4. Under conditions of alkalosis, in which pH increases, the excitability of neurons also increases, rendering them more likely to generate action potentials. This inappropriate stimulation of the nervous system may lead to seizures, particularly in epileptics predisposed to them. Under conditions of acidosis, in which pH decreases, the excitability of neurons is depressed, rendering them less likely to generate action potentials. This lack of nervous system stimulation may lead to a comatose state. Severe diabetic acidosis or acidosis associated with end-stage renal failure will often lead to coma. 

The major characteristics of the renal response to mannitol diuresis include a fall in urine osmolality and a decrease in the osmolality of the interstitial fluid of the renal medulla. The quantity of urine formation and Na excretion is generally proportional to the amount of mannitol excreted. Although there is a significant inhibition of proximal water reabsorption, the effects of mannitol on proximal Na+ reabsorption are not marked. 

Water Flow through an Aquaporin Each human erythrocyte has about 2 X 105 AQP-1 monomers. If water molecules flow through the plasma membrane at a rate of 5 X 10s per AQP-1 tetramer per second, and the volume of an erythrocyte is 5 x 10 n mL, how rapidly could an erythrocyte halve its volume as it encounters the high osmolar-ity (1 m) in the interstitial fluid of the renal medulla Assume that the erythrocyte consists entirely of water. 

Concentration of urine is made possible by generation of osmotic gradients in the renal medulla. This involves a counter-current process which pumps ions without water from the loops of Henle into the medullary interstitial fluid. When the filtrate passes down the collecting ducts lying parallel to the loops of Henle, water passes out of the ducts along an osmotic gradient, provided ADH is present. A hypertonic urine is therefore produced. 

The pathological accumulation of water in the interstitial fluid is called edema. Edema sometimes occurs in the legs. It may be unaesthetic as it results in a puffy appearance, but it can also result in infections. Edema in the air spaces in the lungs can impair breathing. Blood pressure is regulated by hormones that control the resorption of salt. An increased rate of salt resorption results in an increase in water reabsorption by the renal tubule. This is because the water follows the passage of salt by virtue of osmotic forces. The resorption of water is also under the control of vasopressin, as discussed later. 

Elevates osmotic pressure of glomerular filtrate, increases flow of water into interstitial fluid and plasma, inhibiting renal tubular reabsorption of sodium, chloride, producing diuresis. Enhances flow of water from eye into plasma, reducing intraocular pressure (IOP)... 

The more distal portions of the collecting duct pass through the renal medulla, where the interstitial fluid is markedly hypertonic. In the absence of vasopressin, the collecting duct system is impermeable to water, and a dilute urine is excreted. In the presence of vasopressin, the collecting duct system is permeable to water, which is reabsorbed down a steep concentration gradient that exists between the tubular fluid and the medullary interstitium. 

Draw a diagram as you proceed. Indicate the movement of ions from renal tubular fluid to interstitial fluid. Draw arrows to indicate the movements of sodium and chloride ions, making the arrows roughly proportional in length to the amount of the ions reabsorbed. 

Atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP) are members of a family of so-called natriuretic peptides, synthesized predominantly in the cardiac atrium, ventricle, and vascular endothelial cells, respectively (G13, Y2). ANP is a 28-amino-acid polypeptide hormone released into the circulation in response to atrial stretch (L3). ANP acts (Fig. 8) on the kidney to increase sodium excretion and glomerular filtration rate (GFR), to antagonize renal vasoconstriction, and to inhibit renin secretion (Ml). In the cardiovascular system, ANP antagonizes vasoconstriction and shifts fluid from the intravascular to the interstitial compartment (G14). In the adrenal cortex, ANP is a powerful inhibitor of aldosterone synthesis (E6, N3). At the hypothalamic level, ANP inhibits vasopressin secretion (S3). It has been shown that some of the effects of ANP are mediated via a newly discovered hormone, called adreno-medullin, controlling fluid and electrolyte homeostasis (S8). The diuretic and blood pressure-lowering effect of ANP may be partially due to adrenomedullin (V5). 

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