A major renal tubular site of aldosterone action is on the principal cells of the cortical collecting tubule. , Aldosterone increases the sodium permeability of the luminal side of the membrane., Aldosterone increases sodium reabsorption and potassium secretion. , The most important stimuli for aldosterone are increased extracellular potassium concentration and increased angiotensin II. , Aldosterone stimulates the sodium potassium ATPase pump on the basolateral side of the cortical collecting tubule membrane.

The descending limb of Henle’s loop is very permeable to water., The repetitive reabsorption of sodium chloride by the thick ascending loop of Henle and continued inflow of new sodium chloride from the proximal tubule into the loop of Henle is called the countercurrent multiplier., The thick ascending limb is virtually impermeable to water., The active transport of sodium and other ions from the thick ascending loop adds solutes to the renal medullary interstitium. , When the tubular fluid leaves the loop of Henle it has an osmolarity of 100 mOsm/L.

About 25 percent of the filtered loads of sodium, chloride, and potassium are reabsorbed in the loop of Henle, mostly in the thick ascending limb., The thin segment of the ascending limb has a much lower reabsorptive capacity than does the thick segment. , The thick segment of the loop of Henle, is capable of active reabsorption of sodium, chloride, and potassium. , Considerable amounts of calcium, bicarbonate, and magnesium, are reabsorbed in the thick ascending loop of Henle. , The thick segment of the loop of Henle, has thick epithelial cells that have high metabolic activity.

The term alkalosis refers to excess removal of H+ from the body fluids, in contrast to the excess addition of H+, which is referred to as acidosis. , The pH of venous blood and interstitial fluids is about 7.35 because of the extra amounts of CO2 released from the tissues to form H2CO3 in these fluids., The lower limit of pH at which a person can live more than a few hours is about 6.8, and the upper limit is about 8.0., Precise H+ regulation is essential because the activities of almost all enzyme systems in the body are influenced by H+ concentration., The normal pH of arterial blood is 7.4.

Extracellular fluid potassium concentration normally is regulated at about 4.2 mEq/L. , This precise control is necessary because many cell functions are sensitive to changes in extracellular fluid potassium concentration., The redistribution of potassium between the intracellular and extracellular fluid compartments provides a first line of defense against changes in extracellular fluid potassium concentration., Maintenance of balance between intake and output of potassium depends primarily on excretion by the kidneys. , An increase in plasma potassium concentration of only 3 to 4 mEq/L can cause cardiac arrhythmias.

About 80–90% of the HCO3− reabsorption, and H+ secretion, occurs in the proximal tubule., The proximal tubule, thick segment of the ascending loop of Henle, and early distal tubule use sodium-hydrogen exchanger for H+ secretion., CO2, under the influence of the enzyme carbonic anhydrase, combines with H2O to form H2CO3, which dissociates into HCO3− and H+. , The net result is that for every H+ secreted into the tubular lumen, an HCO3− enters the blood., In the thick ascending loop of Henle, another 10% of the filtered HCO3− is reabsorbed.

Calcium ATPase for primary active transport of Ca2+., Sodium-hydrogen exchanger for the secondary active secretion of H+ coupled to Na+ reabsorption, Sodium – potassium ATPase for primary active transport of Na+ in exchange for K+., Sodium glucose co-transporters for secondary active transport of glucose., Hydrogen ATPase for primary active transport of H+ in exchange for K+.

Urinary excretion = Glomerular filtration – Tubular reabsorption + Tubular secretion , It is involving glomerular filtration, It is involving tubular reabsorption, It is involving tubular secretion, For many substances, tubular reabsorption plays a much more important role than secretion in determining the final urinary excretion rate

In the second half of the proximal tubule, sodium is reabsorbed, mainly with chloride ions, The proximal tubule epithelial cells are highly metabolic., In the first half of the proximal tubule, Na+ is reabsorbed by co-transport along with glucose, amino acids, and other solutes., The proximal tubule epithelial cells have large numbers of mitochondria., Proximal tubules have a high capacity for active and passive reabsorption.

In both the proximal tubule and the loop of Henle, a relatively constant fraction of the filtered potassium load is reabsorbed, Most of the day-to-day regulation of potassium excretion occurs in the late distal and cortical collecting tubules, Renal potassium excretion is also determined by the rate of potassium reabsorption by the tubules, Renal potassium excretion is also determined by the rate of potassium filtration., Renal potassium excretion is not determined by the rate of potassium secretion by the tubules

Intracellular H2CO3 dissociates to form CO2, that will be reabsorbed, and H2O, that will be secreted., The net result is that for every H+ secreted into the tubular lumen, an HCO3− enters the blood., Because HCO3– do not permeate the luminal membranes, filtered HCO3– first combines with H+ to form H2CO3, which becomes CO2 and H2O., The transport of HCO3- across the basolateral membrane is facilitated by Na+HCO3− co-transport and Cl−-HCO3− exchanger. , CO2 diffuses into the tubular cell, where it recombines with H2O, under the influence of carbonic anhydrase, to generate H2CO3.

Increases in sodium intake causes volume expansion, and small increases in arterial pressure that raise sodium excretion through pressure natriuresis., Activation of low-pressure receptor reflexes inhibits sympathetic nerve activity to the kidneys to decrease tubular sodium reabsorption, Stimulation of natriuretic systems, especially ANP, contributes further to increased sodium excretion, Increased arterial pressure suppressed Ang II stimulatory effect on aldosterone secretion, reducing tubular sodium reabsorption, Increased arterial pressure suppressed Ang II formation and eliminates its direct stimulatory effect tubular sodium reabsorption

The transport maximum is due to saturation of the specific transport systems involved., Normally, measurable glucose does not appear in the urine because essentially all the filtered glucose is reabsorbed in the proximal tubule. , The transport maximum appears when the tubular load exceeds the capacity of the carrier proteins involved in the transport process. , When the filtered load exceeds the capability of the tubules to reabsorb glucose, urinary excretion of glucose does occur

Some parts of the tubule, especially the proximal tubule., Reabsorption of large molecules such as proteins , An active transport mechanism for reabsorption of proteins., Once inside the cell, the protein is digested into its constituent amino acids, which are reabsorbed through the basolateral membrane into the interstitial fluid., The protein attaches to the brush border of the luminal membrane, and this portion of the membrane then invaginates until.

In the ascending limb of the loop of Henle, especially in the thick segment, sodium, potassium, and chloride are avidly reabsorbed. , In healthy kidneys, fluid leaving the ascending loop of Henle and early distal tubule is always dilute., When the glomerular filtrate is initially formed, its osmolarity is about the same as that of plasma (300 mOsm/L)., As fluid flows through the proximal tubule, solutes and water are reabsorbed in equal proportions, so little change in osmolarity occurs., Tubular fluid in distal and collecting tubules is further diluted in the presence of ADH.

The thick segment of the ascending limb of the loop of Henle empties into the distal tubule., The early distal tubule reabsorbs sodium, chloride, calcium, and magnesium but is virtually impermeable to water and urea. , The macula densa provides feedback control of GFR and blood flow in this same nephron., The first portion of the distal tubule forms the macula densa., The macula densa is a group of closely packed epithelial cells.

The H+, from H2CO3 dissociation, is secreted into the tubule by means of the hydrogen-ATPase and the hydrogen-potassium-ATPase transporters., The secretion of H+ in the late distal tubule and collecting tubules is important in forming maximally acidic urine., H+ secretion in the type A intercalated cells starts with intracellular CO2 that combine with H2O to form H2CO3 which dissociates to H+ and HCO3–. , At the luminal membrane of the tubular cell, H+ is transported directly by a hydrogen-transporting ATPase and a hydrogen-potassium-ATPase transporter. , Primary active secretion of H+ occurs in the type A intercalated cells of the late distal tubule and in the collecting tubules

The proximal tubules reabsorb essentially all the filtered glucose and amino acids., The proximal tubules reabsorb about 65% percent of the filtered sodium, chloride, bicarbonate, and potassium., The proximal tubules secrete organic acids, bases, and hydrogen ions into the tubular lumen., The Na+/K+ ATPase provides the major force for reabsorption of Na+, Cl-, and H2O throughout the proximal tubule. , The osmolarity is reabsorbed mainly in first half of the proximal tubule.

The primary mechanism for removal of nonvolatile acids from the body is renal excretion., Under normal conditions, almost all filtered HCO3- is reabsorbed from the tubules., The kidneys must prevent the loss of bicarbonate in the urine., The kidneys control acid-base balance by excreting either acidic or basic urine, The kidneys are by far the most powerful of the acid-base regulatory systems.

The vasa recta carry away only as much solute and water as is absorbed from the medullary tubules, preserving the high osmolarity of medulla., The osmolarity of interstitial fluid in almost all parts of the body is about 300 mOsm/L., The high solute concentration in the medulla is maintained by a balanced inflow and outflow of solutes and water in the medulla., The renal medullary interstitium has accumulated solutes in great excess of water. , The osmolarity of the interstitial fluid in the pelvic tip of the medulla may increase to 1200 to 1400 mOsm/L.

The reabsorption of solutes in the thick segment of the ascending loop of Henle is closely linked to the activity of the Na+/K+ ATPase pump., The thick ascending limb of the loop of Henle is the site of action of the “loop” diuretics., In the thick ascending loop, movement of sodium across the luminal membrane is mediated primarily by a 1-sodium, 2-chloride, 1-potassium co-transporter., The 1-sodium, 2-chloride, 1-potassium co-transporter transport potassium into the cell against a concentration gradient., An important component of solute reabsorption in the thick ascending limb is the sodium-potassium ATPase pump.

10% of the filtered glucose is reabsorbed by SGLT1 in the latter segments of the proximal tubule. , SGLT carry glucose into the cell cytoplasm against a concentration gradient. , 90% of the filtered glucose is reabsorbed by SGLT2 in the early part of the proximal tubule (S1 segment). , SGLT are located on the brush border of proximal tubular cells, On the basolateral side of the membrane, glucose diffuses out of the cell into the interstitial spaces with the help of glucose transporters GLUT

Sympathetic nervous system effects occur by activation of α-adrenergic receptors on the renal tubular epithelial cells., Severe activation of the sympathetic nervous system, decreases sodium excretion by constricting the renal arterioles and reducing the GFR. , Even low levels of sympathetic activation, increasing sodium reabsorption in the proximal tubule, the thick ascending limb of the loop of Henle, and perhaps in more distal parts of the renal tubule. , Sympathetic nervous system increases renin release and angiotensin II formation, which further increase tubular sodium reabsorption. , Sympathetic nervous system activation increases sodium reabsorption.

The tubular membranes of both segments are almost completely impermeable to urea., Both segments reabsorb Na+ and secrete K+., The rate of Na+ reabsorption in both segments is controlled by aldosterone. , The permeability to water is controlled by the concentration of ADH., The intercalated cells play a key role in acid-base regulation of the body fluids.

The sodium-potassium ATPase pump brings potassium into the cell. , The sodium-potassium ATPase pump favors sodium diffusion into the cell through special channels. , From in the cell, potassium diffuses down its concentration gradient across the luminal membrane into the tubular fluid. , The sodium-potassium ATPase pump in each cell’s basolateral membrane maintains a low sodium concentration inside the cell. , The sodium is secreted in the urine by fast voltage-gated Na+ channels.

ADH allows the distal tubules and collecting ducts to avidly reabsorb water. , The basic requirements for forming a concentrated urine include a high osmolarity of the renal medullary interstitial fluid., The renal medullary interstitium surrounding the collecting ducts is normally hyperosmotic. , The renal medullary interstitial fluid, provides the osmotic gradient necessary for water reabsorption to occur in the presence of high levels of ADH., The basic requirements for forming a concentrated urine include a high level of ADH.

Water, chloride, and urea reabsorption are coupled with sodium reabsorption, The most important of the secondary active transport processes for chloride reabsorption involves co-transport of chloride with sodium across the luminal membrane., Na+ reabsorption → H2O reabsorption → ↑ Luminal urea concentration → Passive urea reabsorption, Na+ reabsorption → ↑ Lumen negative potential → Passive Cl– reabsorption, Na+ reabsorption → H2O reabsorption → ↑ Luminal Cl– concentration → Passive Cl– reabsorption

For sodium, chloride, and bicarbonate rates of reabsorption are depending on the needs of the body. , Tubular reabsorption is highly selective., Tubular reabsorption = Glomerular filtration + Tubular secretion – Urinary excretion, Waste products, such as urea and creatinine, are poorly reabsorbed from the tubules , Glucose and amino acids, are almost completely reabsorbed from the tubules.

The intrinsic ability of the tubules to increase their reabsorption rate in response to increased tubular load. , It acts as a line of defense to buffer the effects of spontaneous changes in GFR on urine output., It helps to prevent overloading of the distal tubular segments when GFR increases. , It is a mechanism that promotes large changes in fluid flow in the distal tubules when the arterial pressure change. , It can occur independently of hormones.

↑ HCO3−, Hyperkalemia, ↓ PCO2, ↓ Angiotensin II, ↓ Aldosterone

Increased tubular flow rate, stimulates potassium secretion by the principal cells., In circumstances associated with severe potassium depletion, there is a net reabsorption of potassium by the type A intercalated cells., Increased aldosterone, stimulates potassium secretion by the principal cells., Increased extracellular fluid potassium concentration, stimulates potassium secretion by the principal cells. , Increased hydrogen ion concentration, decreases potassium secretion.

Alkalosis → decrease extracellular [K+] , β-adrenergic stimulation → decrease extracellular [K+], Acidosis → increase extracellular [K+], Cell lysis → increase extracellular [K+], Increased extracellular fluid osmolarity → increase extracellular [K+]

The osmolarity in the extracellular fluid must be precisely regulated to prevent the cells from shrinking or swelling., When there is excess water in the body and body fluid osmolarity is reduced, the kidneys can excrete urine with a very low osmolarity. , The total body water is partially controlled by fluid intake, which is regulated by factors that determine thirst., To a large extent, extracellular fluid osmolarity and sodium chloride concentration are regulated by the amount of extracellular water., The total body water is partially controlled by renal water excretion, which is controlled by factors influencing glomerular filtration and tubular reabsorption.

It is virtually impermeable to water and urea., It is referred to as the diluting segment because. , There is a sodium-chloride co-transporter., It avidly reabsorbs most of the ions, including sodium, potassium, and chloride. , Approximately 5 percent of the filtered load of sodium chloride is reabsorbed.

ADH is an effector for the feedback system that controls plasma osmolarity by altering renal excretion of water independently of the rate of solute excretion. , Antidiuretic hormone (ADH), is also called vasopressin., The rate of ADH secretion determines whether the kidney excretes dilute or concentrated urine. , ADH increases water reabsorption and decreases urine volume but does not markedly alter the rate of renal excretion of the solutes. , When osmolarity of the body fluids increases above normal, the posterior pituitary gland secretes ADH

The principal cells reabsorb sodium from the lumen and secrete potassium ions into the lumen., Type A intercalated cells secrete hydrogen ions into the lumen., Type A intercalated cells reabsorb potassium and bicarbonate ions from the lumen., The reabsorption of water from this tubular segment is controlled by the antidiuretic hormone., The late distal tubules and cortical collecting tubules are composed of two distinct cell types, the principal cells, and the intercalated cells.

An increase in resistance of either the afferent or the efferent arterioles reduce peritubular capillary hydrostatic pressure and tends to increase reabsorption rate. , Increases peritubular capillary hydrostatic pressure tends to decrease reabsorption rate. , Increases in arterial pressure tend to raise peritubular capillary hydrostatic pressure and decrease the reabsorption rate., A decrease in efferent arteriolar resistances increases peritubular capillary hydrostatic pressure and tends to decrease reabsorption rate. , A decrease in afferent arteriolar resistance increases peritubular capillary hydrostatic pressure and tends to decrease reabsorption rate.

Angiotensin II → Proximal tubule, thick ascending loop of Henle/distal tubule, collecting tubule , Antidiuretic hormone → Distal tubule/collecting tubule and duct , Parathyroid hormone → Proximal tubule, thick ascending loop of Henle/distal tubule, Aldosterone → Collecting tubule and duct , Atrial natriuretic peptide → Distal tubule/collecting tubule and duct

Are the final site for processing the urine. , The permeability of the medullary collecting duct to water is controlled by the level of ADH., Reabsorb less than 10% of the filtered water and sodium., There are special urea transporters that facilitate urea diffusion. , Are capable of secreting H+ against a large concentration gradient.

Angiotensin II → ↓ the renal plasma flow → ↑ filtration fraction → ↑ the peritubular capillary reabsorption, ↑ the plasma protein concentration of systemic blood → ↑ the peritubular capillary colloid osmotic pressure → ↑ the peritubular capillary reabsorption. , ↑ the filtration fraction → ↑ the peritubular capillary colloid osmotic pressure → ↑ the peritubular capillary reabsorption rate., ↑ of peritubular capillary filtration coefficient → ↑ the peritubular capillary reabsorption rate. , ↑ the colloid osmotic pressure of the plasma in peritubular capillaries → ↑ the peritubular capillary reabsorption.

The normal rate of peritubular capillary reabsorption is about 124 ml/min., The net reabsorptive pressure is normally about 10 mm Hg, causing fluid and solutes to be reabsorbed into the peritubular capillaries. , The large filtration coefficient is a result of a high hydraulic conductivity and large surface area of the capillaries. , Fluid and electrolytes are reabsorbed from the tubules into the renal interstitium and from there into the peritubular capillaries., As the glomerular filtrate passes through the renal tubules, more than 99% of the water and most of the solutes are normally reabsorbed.

Amino acids, Urate, Lactate, Phosphate, Glucose

Passive water reabsorption by osmosis is coupled mainly to sodium reabsorption. , As water moves across the tight junctions by osmosis, it can also carry with it some of the solutes, a process referred to as solvent drag., A large part of the osmotic flow of water in the proximal tubules occurs through the tight junctions between the epithelial cells., The proximal tubule is highly permeable to water., In the proximal tubule water is reabsorbed as rapidly as the solutes

↑ Angiotensin II , ↑ PCO2 , Hypokalemia, ↓ Extracellular fluid volume, ↓ Aldosterone

Aldosterone deficiency → shifts K+ out of cells, Insulin deficiency → shifts K+ out of cells., Aldosterone → shifts K+ into cells, β-adrenergic blockade → shifts K+ out of cells., Insulin → shifts K+ into cells

The luminal membrane of the principal cells is highly permeable to potassium, The increase of plasma aldosterone concentration stimulates potassium secretion by the principal cells of the cortical collecting tubules., Potassium channels abundance in the luminal membrane is increased during high potassium intake. , In the late distal and cortical collecting tubules, cells that secrete potassium are called principal cells., The luminal membrane of the principal cells has the renal outer medullary potassium channels, and high conductance “big” potassium channels.

Atrial natriuretic peptide → ↓ NaCl reabsorption , Angiotensin II → ↑ NaCl, H2O reabsorption, ↑ H+ secretion , Antidiuretic hormone → ↑ H2O reabsorption, Aldosterone → ↑ NaCl, H2O reabsorption, ↑ K+ secretion, ↑ H+ secretion , Parathyroid hormone → ↓ PO4− reabsorption, ↑ Ca++ reabsorption

Stimulate sodium-bicarbonate co-transport in the basolateral membrane. , Stimulates aldosterone secretion., Constricts the efferent arterioles., Stimulate the sodium-potassium ATPase pump on the tubular epithelial cell basolateral membrane. , Stimulate sodium-hydrogen exchange in the luminal membrane, especially in the proximal tubule.

Most of the water delivered to this segment remains in the tubule despite reabsorption of large amounts of solute., The “loop” diuretics stimulates the action of the sodium, 2-chloride, potassium cotransporter., The tubular fluid in the ascending limb becomes very dilute as it flows toward the distal tubule., The thick segment of the ascending loop of Henle is virtually impermeable to water., In the thick ascending limb, there is a significant paracellular reabsorption of cations, such as Mg++, Ca++, Na+, and K+.

The average person can clear 90% of the para-aminohippuric acid from the plasma flowing through the kidneys and excrete it in the urine., The proximal tubule is an important site for secretion of organic acids and bases., Kidneys secrete many potentially harmful drugs or toxins directly through the tubular cells., The proximal tubule is also an important site for secretion of bile salts, oxalate, urate, and catecholamines. , Creatinine concentration increase along the proximal tubule.

After eating a meal that contains large amounts of salt and water → reflex inhibition of renal sympathetic activity → rapid elimination of excess fluid., Hemorrhage → ↓ blood volume →reflex activation of the sympathetic nervous system →↓ sodium and water excretion → the rapid restitution of blood volume. , ↑ renal sympathetic nerve activity →↑ constriction of the renal arterioles →↓ GFR →↓ sodium and water excretion. , ↑ renal sympathetic nerve activity →↑ renal sympathetic nerve activity ↑ renal sympathetic nerve activity →↑ tubular reabsorption of salt and water., ↑ renal sympathetic nerve activity →↑ renin release →↑ Ang II and aldosterone formation →↑ tubular reabsorption of sodium and water.

Type B intercalated cells have hydrogen and bicarbonate transporters on the basolateral membrane., Type A cells secrete H+ while reabsorbing HCO3- and K+ in acidosis, In these cells, by the action of carbonic anhydrase on H2O and CO2 the H2CO3 is formed, which then dissociates into H+ and HCO3-., Type A cells contain hydrogen-ATPase and hydrogen/potassium-ATPase in the luminal membrane. , Type B cells reabsorb H+ while secreting HCO3- and K+ in alkalosis.

Metabolic acidosis increases extracellular potassium concentration, in part by causing loss of potassium from the cells , Epinephrine stimulates potassium uptake into cells, mainly by activation of β2adrenergic receptors., Treatment of hypertension with β-adrenergic receptor blockers, causes potassium to move out of the cells. , During prolonged exercise, potassium is released from skeletal muscle into the extracellular fluid. , Insulin is important for increasing cell potassium uptake after a meal.

The more concentrated the urine, the higher the urine specific gravity., The urine specific gravity increases linearly with increasing urine osmolarity., Urine specific gravity is often used in clinical settings to provide a rapid estimate of urine solute concentration. , Urine specific gravity normally ranges from 1.002 to 1.028 g/ml. , Presence of glucose could increase the measured values of urine specific gravity despite a normal urine osmolality.

Recirculation of urea from the collecting duct to the loop of Henle., Diffusion of only small amounts of water from the medullary tubules into the medullary interstitium, Active transport of sodium ions and co-transport of potassium, chloride, and other ions out of the thick portion of the ascending limb of the loop of Henle into the medullary interstitium. , Active transport of ions from the collecting ducts into the medullary interstitium. , Facilitated diffusion of urea from the inner medullary collecting ducts into the medullary interstitium.

When high levels of ADH are present, the fluid at the end of the collecting ducts has osmolarity about 1200 mOsm/L , In the medullary collecting ducts, the water shifts from the tubular fluid into the interstitium., The reabsorbed water is carried away by the vasa recta into the venous blood., In the cortical collecting tubule, the amount of water reabsorbed is dependent on the plasma concentration of ADH., The passive transport of ions from the thick ascending loop adds solutes to the renal cortex.

Type A intercalated cells are especially important in eliminating hydrogen ions while reabsorbing bicarbonate in acidosis. , In the collecting tubules and collecting ducts, there are two types of intercalated cells, type A and type B., Type A intercalated cells secrete hydrogen ions by a hydrogen-ATPase transporter and by a hydrogen-potassium-ATPase transporter. , Intercalated cells are not important for acid-base regulation. , Type B intercalated cells secrete bicarbonate into the tubular lumen while reabsorbing hydrogen ions in alkalosis.

When there is a reduction in the extracellular fluid H+ concentration (alkalosis), the kidneys secrete less H+ and fail to reabsorb all the filtered HCO3−. , In acidosis, the kidneys secrete additional H+ and reabsorb all the filtered HCO3− and produce new HCO3−., The kidneys regulate extracellular fluid H+ concentration partially by production of new HCO3−. , The kidneys regulate extracellular fluid H+ concentration partially by secretion of H+. , The kidneys regulate extracellular fluid H+ concentration partially by reabsorption of filtered HCO3−.

About 20% of the filtered water is reabsorbed in the thin descending limb of the loop of Henle., The loop of Henle consists of three functionally distinct segments: the thin descending segment, the thin ascending segment, and the thick ascending segment., The thin descending and thin ascending segments, as their names imply, have thin epithelial membranes with no brush borders. , The descending part of the thin segment is highly permeable to water., The ascending limb, is virtually impermeable to water.

Enormous increases in arterial pressure can cause irrelevant variation in urinary excretion of sodium., Even small increases in arterial pressure can cause marked increases in urinary excretion of water, a phenomenon called pressure diuresis, Even small increases in arterial pressure can cause marked increases in urinary excretion of sodium, a phenomenon called pressure natriuresis. , ↑ arterial pressure →↓ angiotensin II formation →↓ tubular sodium reabsorption , Increasing the arterial pressure between 75 -160 mm Hg usually has only a small effect on renal blood flow and GFR.

When the plasma glucose concentration is 100 mg/100 ml there is no loss of glucose in the urine, The overall transport maximum for the kidneys, is reached when all nephrons have reached their maximal capacity to reabsorb glucose., When the plasma concentration of glucose rises above about 200 mg/100 ml, a small amount of glucose begins to appear in the urine., The appearance of glucose in the urine occurs after the transport maximum is reached, Not all nephrons have the same transport maximum for glucose.

AVP binds to its V2 receptors. , The molecules of aquaporin-2 fuse together to form water channels on the luminal side of the cell membrane. , Activated PKA phosphorylates intracellular proteins, causing movement of aquaporin-2 to the luminal side of the cell membrane. , V2 receptors are coupled with GS proteins that activate adenylate cyclase and stimulate formation of cAMP that activates protein kinase A, The aquaporins from the basolateral side of the cell membrane (AQP-3 and AQP-4) permit water to flow out of the cell on.

The maximal concentrating ability of the kidney dictates the obligatory urine volume., The ability of the kidneys to form a small volume of concentrated urine minimizes the intake of fluid required to maintain homeostasis. , The human kidney can produce a maximal urine concentration of 1200 to 1400 mOsm/L. , The ability of the kidney to form urine more concentrated than plasma is essential for survival. , For a normal 70-kilogram human with a maximal urine concentrating ability of 1200 mOsm/L, the obligatory urine volume is 0.5L/day.

The excess H+ combines with HPO42– to form H2PO4−, that can be excreted as NaH2PO4., The most important buffers in the tubular fluid are phosphate buffer and ammonia buffer. , When H+ is secreted in excess of the HCO3− filtered into the tubular fluid, only a small part of the excess H+ can be excreted as (H+) in the urine. , Glutamine is metabolized in the tubular cell, yielding two NH4+ (will be secreted) and two HCO3− (will be reabsorbed), The excretion of large amounts of H+ in the urine is accomplished primarily by combining the H+ with buffers in the tubular fluid.