Renal & Urinary System Physiology-Review & Illustrations
Renal functions:
- Kidneys regulate water and electrolytes balance
- Kidneys responsible for excretion of metabolic waste products
- Kidneys play essential role in regulation of arterial pressure
- Kidneys contribute to acid-base regulation
- Kidneys responsible for regulation of erythrocyte production from the bone marrow
- Kidneys regulate 1, 25- dihydroxy vit D3 production
- In kidneys, gluconeogenesis can take place
Functional anatomy of nephron
Bowman`s capsule
- It is the invaginated blind end of the tubule that
encased the glomerulus (which is a branching capillaries).
- The
pressure in the glomerular capillaries is higher than that in other capillary
beds.
- The membrane of the glomerular capillaries is called the
glomerular membrane.
The average total area of glomerular capillary endothelium across which
filtration occurs (i.e. the glomerular membrane) is about 0.8 m2.
- In general, the glomerular membrane is different from other capillary membranes by having three layers instead of two. These three layers are endothelial layer of the capillary itself, a basement membrane (basal lamina), and a layer of epithelial cells (podocytes).
- The permeability of the glomerular membrane is from 100-500 times as great as that of the usual capillary.
This thick ascending segment ascends all the way back
to the same glomerulus from which the tubule originated and passes tightly
through the angle between the afferent and efferent arterioles. The cells of this
portion of the thick ascending segment which are in complete attachment with
the epithelial cells of the afferent and efferent arterioles are called Macula
densa. The specialized smooth muscle cells of the afferent
arterioles that come in contact with the macula densa are called juxtaglomerular
cells (JG cells) which contain renin granules. Macula densa
and JG cells plus few granulated cells between them are collectively known as
juxtaglomerular complex or apparatus which has a dense
adrenergic neural innervation.
[A] Proximal tubules
- Proximal tubule reabsorption (see also figure)
- The epithelial cells of the proximal tubule are highly metabolic cells, with large number of mitochondria to support extremely rapid active transport processes and they are united by apical tight junction but contain lateral intercellular space. It contains a brush border due to the presence of microvilli.
- About 65% of filtered NaCl, K+, and tubular H2O are reabsorbed in proximal tubule. This is the site for the action of osmotic diuretics such as mannitol. Carbonic anhydrase inhibitors (e.g., acetazolamide)
are diuretics that act in the early proximal tubule by inhibiting the
reabsorption of filtered HCO3-
. Osmotic diuretics are non-reabsorbed solutes present in the tubule
lumen; they cause water to remain in the lumen and to be passed into the
urine. An example of osmotic diuresis is untreated diabetes mellitus,
when the glucose Tm is exceeded and glucose remains in the tubule lumen.
The proximal tubule and thin descending limb of the loop of Henle are
the main sites of action because these areas have the highest membrane
water permeability and are affected most by osmotic gradients. The inert
sugar mannitol can be used to clinically induce an osmotic diuresis.
Mannitol can be helpful in the treatment of patients with head injuries
to reduce intracranial pressure by producing a fluid shift out of the
brain. Because of their weak diuretic effect, carbonic anhydrase
inhibitors are rarely used for this purpose. Acetazolamide is commonly
used in the treatment or prophylaxis of altitude sickness and in
reducing intraocular pressure associated with glaucoma.
- Although the amount of Na in the tubular fluid decreases markedly along the proximal tubule, the concentration of Na and the total osmolarity remains relatively constant (isotonic).
- Reabsorption of HCO3- occurs primarily in the proximal tubule indirectly through the absorption of CO2 from proximal tubular fluid.
- The proximal tubule epithelium also secretes H+, organic acids, bases, and certain drugs.
- The proximal tubule is the site of glomerulotubular balance.
[B] Loops of Henle
According to the location of loop of Henle, nephrons can be classified into:
- Cortical nephrons, 70%, have short loops of Henle, its loop is located mainly in the renal cortex.
- Juxtamedullary nephrons, 30%, have long loops of Henle, its loop dips deep down into the renal medulla.
- Important for urine concentration,
- Reabsorb a higher proportion of glomerular filtrate than cortical nephrons “salt-conserving nephrons”.
- In states where effective circulating blood
volume is
reduced, a higher proportion of renal blood flow (RBF) is directed to the
juxtamedullary nephrons, helping to conserve extracellular fluid volume.
The thin descending segment of the loop of Henle
- The epithelia cells of it are very thin with no
brush border and very few mitochondria.
- They are highly permeable to water
- Nearly
impermeable to sodium and most other ions.
The thin ascending segment of the loop of Henle
- Impermeable to
water, no water reabsorption is taking place in this area of the nephrone.
- Permeable to urea and NaCl than is the descending
portion.
The thick ascending segment of
the loop of Henle
- The
epithelial cells of the ascending thick segment are similar to those of the
proximal tubules except that they have a rudimentary brush border and much
tighter tight junction.
- The cells adapted for strong active transport of Na, K, and Cl ions. About 20% of the filtered NaCl is reabsorbed in this region. This active transport of ions can be inhibited by
drugs called loop diuretics such as frusemide, ethacrynic acid, and bumetanide.
Because of their powerful diuretic effect, loop diuretics are
particularly useful when diuresis is needed (e.g., pulmonary edema).
- Impermeable to water and urea. Therefore, no water reabsorption is taking place in this area of the nephrone "the diluting segment".
- It is the only segment in which active Cl pumping occur.
[C] Distal convoluted tubule
The "early" distal convoluted tubule- Has almost the same characteristics as the thick
segment of ascending limb of the loop of Henle.
- It reabsorbs Na ions and other ions "diluting segment".
- Impermeable
to both water and urea.
- This segment is the site of action of special type
of diuretics called thiazide diuretics.
Thiazide diuretics (e.g., hydrochlorothiazide) inhibit Na-Cl
cotransport in the early distal tubule. Thiazides are less potent loop
diuretics because a lower proportion of the filtered load is reabsorbed
in the distal tubule compared to the loop of Henle. Thiazides are
considered first-line agents in the treatment of hypertension, but they
can also be used in a variety of conditions, including symptomatic
relief of edema and calciuria.
- Most abundant cells
- Responsible for NaCl reabsorption and K+ excretion (under the effect of aldosterone)
- Responsible for reabsorption of water (under the effect of ADH)
- Alpha-intercalated cells (which secrete Acid, i.e. H+) and,
- Beta-intercalated cells (which secrete Base, i.e. HCO3–)
- Na ions reabsorption while secrete K ions under the effect of aldosterone through increase the activity of Na-K ATPase countertransporter.
- Vasopressin-stimulated water reabsorption. Its permeability to water is under the control of
ADH similar to the cortical collecting duct.
- H ions secretion and bicarbonate ions transport (by H-ATPase pump) under the effect of aldosterone.
- About 3% of NaCl is reabsorbed in this part of tubule.
- It is permeable to urea (unlike the cortical collecting duct) which is increased in the presence of ADH.
- It is the site for K+-sparing diuretics such as Spironolactone which is an antagonist of aldosterone. It decreases K+ secretion. If used alone, they cause hyperkalemia. Agents that act
on the principal cells in the cortical collecting duct are called K+-sparing
diuretics because inhibition of reabsorption at this site also
inhibits K+
secretion. Amiloride is an example of
this class of diuretic, which acts by blocking apical Na+ channels in
the
principal cells. Aldosterone antagonists (e.g., spironolactone) belong
to the
group of K+-sparing diuretics and act by reducing the expression and
activity
of Na+ transport proteins in the cortical collecting duct. K+-sparing
agents have a weak diuretic effect
because less than 5% of filtered Na+ is reabsorbed at this site. However,
agents
in this group can be helpful in the treatment of certain specific
disorders.The most important use of the K+-sparing diuretics is in
combination with thiazide or loop diuretics to offset (reduce) urinary
K+ losses.
Osmolarity of tubal & interstitial fluid
At each horizontal level, the medullary
interstitium is concentrated by the transport of solute from the ascending loop
of Henle as the descending loop of Henle is freely water permeable, i.e water passively
leaves the tubule concentrating the luminal contents. These two processes
proceed at each horizontal level so that the final concentration of solute deep
in the medullary interstitium is ~ 1200-1400 mosmol/l. The gradient at each
horizontal level across the ascending loop of Henle (see A of the figure) remains at only 200
mosmol/l, while that across the descending loop of Henle is near zero
(see B of the figure) therefore, the osmolality in the ascending loop of Henle is always less than
that of the descending loop of Henle. The fluid leaving the thick ascending loop
of Henle for the distal tubule is ~ 200
mosmol/l below plasma, ie. ~ 100 mosmol/l.
Blood
vessels (see also figure):
- The renal fraction of the
total cardiac output is about 25% .
- In resting adult, the
blood flow in renal cortex is about 98% of the total renal blood flow while in
renal medulla is only 2% of the total renal blood flow. This is why the O2
consumption of cortex is much higher than that of medulla.
- Arterial system of the kidney is technically a portal system, because branches twice.
- In the juxtamedullary glomeruli, long efferent arterioles extend from the glomeruli down into the outer medulla and then divide into specialized long and straight capillary loops called vasa recta extended downward into the medulla to lay side by side with the lower parts of thin segments of juxtaglomerular loops of Henle all the way to the renal papillae. Then, like the loop of Henle, they also loop back toward the cortex and empty into the cortical veins. This specialized network of capillaries in the medulla plays an essential role in the formation of concentrated urine. The shape and the arrangement of the loop of the vasa recta capillaries allows the blood to run parallel to and opposite to the flow of the fluid in the loop of Henle.
- Vasoconstriction of renal arterioles, which leads to a decrease in Renal Blood Flow (RBF), is produced by activation of the sympathetic nervous system and angiotensin II. At low concentrations, angiotensin II preferentially constricts efferent arterioles, thereby “protecting” (increasing) the GFR.
Angiotensin-converting enzyme (ACE) inhibitors dilate efferent
arterioles and produce a decrease in GFR; these drugs reduce
hyperfiltration and the occurrence of diabetic nephropathy in diabetes
mellitus.
■ Vasodilation of renal arterioles, which leads to an increase in RBF, is produced by
prostaglandins E2 and I2, bradykinin, nitric oxide, and dopamine.
Nerve supply:
The kidney has a rich adrenergic sympathetic nerve (there is no significant parasympathetic innervation) supply distributed to the:
- Vascular smooth muscle to cause vasoconstriction (through alpha 1 receptors) .
- Juxtaglomerular cells to cause renin secretion (through beta 1 receptors) .
- Tubular cells to stimulate Na and water reabsorption (through alpha and beta receptors).
Glomerular filtration rate (GFR)
It is the fluid that filtrate through the glomerulus into
Bowman`s capsule each minute in all nephrons of both kidneys
which is about 125 ml/min or
180 L/day in
males (10% lower in female). Despite the tremendous permeability of the
glomerular membrane, it has an extremely high degree of selectivity. The
selectivity of the glomerular membrane depends on:
- Size of the molecules
- The electrical charges of the molecules
The composition of the glomerular filtrate is the same as plasma except that it has no significant amount of proteins.
The filtration fraction
is the fraction of the renal plasma flow that becomes glomerular filtrate. Since the normal plasma flow through both kidneys is 650 ml/min and the normal GFR is 125 ml/min, the average filtration fraction is about 1/5 or 19%.
Renal clearance:
Is the volume of blood plasma from which a particular waste is completely removed in 1 minute. It represents the net effect of three processes: Glomerular filtration of the waste + Amount added by tubular secretion - Amount reclaimed by tubular reabsorption.
C= UV/P, where:
C = clearance (mL/min or mL/24 hr)
U = urine concentration (mg/mL)
V = urine volume/time (mL/min mL/24 hr)
P = plasma concentration (mg/mL)
Example: The following values were obtained for urea: U (urea concentration in urine) = 6.0 mg/mL, V (rate of urine output) = 2 mL/min, P (urea concentration in plasma) = 0.2 mg/mL.
Renal clearance (C) is C = UV/P = (6.0 mg/mL) (2 mL/min)/ 0.2 mg/mL = 60
mL/min. This means that 60 mL of blood plasma is completely
cleared of urea per minute. If this person has a normal GFR of 125 mL/min, then
the kidneys have cleared urea from only 60/125 = 48% of the glomerular
filtrate.
Using clearance to estimate GFR: The substance is called glomerular filtration marker. The substance used as glomerular filtration marker to
measure the clearance should fulfill the following criteria:
- Freely filtered.
- Neither reabsorbed nor secreted by the tubules.
- Not metabolized or stored in the kidney.
- Not toxic and not affecting the GFR.
Such of these substances are inulin, creatinine, and para-aminohippuric acid.
In clinical practice, GFR is more often estimated from creatinine
excretion. This has a small but acceptable error of measurement, and is
an easier procedure than injecting inulin and drawing blood to measure
its concentration.
Using clearance to estimate renal blood flow (RBF):
Para-aminohippuric acid (PAH) clearance is used as a measure of renal
blood (plasma) flow (RPF): PAH, like inulin and creatinine in its
criteria. However, PAH is different from inulin and creatinine in that
it is cleared from the plasma by a single passage through the kidney
and the remaining PAH in the plasma after the glomerular filtrate is
formed, is secreted into the tubules by the proximal tubule, i.e. zero
PAH in renal vein.
GFR can be affected by
[1]: The filtration pressure, which is influenced by:
- Renal
blood flow. Increase blood flow through the nephrons greatly increases
the GFR for two reasons: (A) The increasing flow increases the
glomerular pressure which enhances filtration. (B) The increased flow
through the nephrons allows less time for plasma proteins to be more
concentrated at the venous end of the glomerular capillaries bed.
Therefore, oncotic pressure has far less inhibitory influence on
glomerular filtration.
- Afferent arteriolar constriction.
- Efferent arteriolar constriction. A slight efferent arteriolar constriction increases the
glomerular pressure causing slight increase in GFR. However, moderate and
severe efferent arteriolar constriction causes a paradoxical decrease in
the GFR despite the elevated glomerular pressure. This is due to the fact that
plasma in this case will remain for long period of time in the glomerulus, and
extra large portion of plasma will filter out. This will increase the plasma
colloid osmotic pressure to excessive level causing a decrease in the GFR.
C. Glomerular capillary colloid osmotic pressure.
D. Bowman’s colloid osmotic pressure.
[2]: The capillary filtration coefficient (Kf), which can be affected by:
A. The
permeability of the glomerular capillaries. Normally, anionic
glycoproteins line the filtration barrier restrict the filtration of
plasma proteins, which are also negatively charged. In glomerular
disease, the anionic charges on the barrier may be removed, resulting in
proteinuria.
B. The thickness and surface area of capillary bed.
Therefore, the factors that determine the final urine volume are the following:
[1] Presence of excessive quantities of osmotic particles
(Osmotic diuresis) due to the presence of non-absorbed osmotic
particles in tubules such as glucose, sucrose, mannitol, and urea.
[2] Plasma colloid osmotic pressure:
A sudden increase in plasma colloid osmotic pressure instantaneously
decreases the rate of fluid volume excretion. The cause of this is due
to (A) a decrease in GFR and (2) an increase tubular reabsorption.
[3] Sympathetic stimulation:
Sympathetic stimulation preferentially causes constriction of the
afferent arterioles via α1 receptors stimulation. It greatly decreases
the glomerular pressure and simultaneously decreases GFR. At the same
time, the blood flow into the peritubular capillaries is decreased and
consequently, the capillary pressure is decreased, thus increasing
tubular reabsorption. Also sympathetic stimulation stimulate
juxtaglomerular complex (via β1 receptors) to release renin.
[4] Arterial pressure:
Under normal condition (when the renal autoregulatory mechanism is
intact), a change in blood pressure causes a slight change diuresis and
natriuresis. Unlike in renal diseases (when the renal autoregulatory
mechanism is impaired), small increase in arterial pressure often causes
marked increase in urinary excretion of Na and water. This results from
two separate effects: (A) the increase in arterial pressure increases
glomerular pressure, which in turn increases GFR, thus leading to
increased urine output. (B) The increase in arterial pressure also
increases the peritubular capillary pressure, thereby decreasing tubular
reabsorption.
[5] Hormonal control: Such as:
- ADH: When excess antidiuretic hormone is secreted by the posterior pituitary gland, the effect is to increase the water permeability of the distal tubule, collecting tubule and collecting duct with a consequent decrease the urinary volume output acutely. However, when excess ADH is secreted for long periods of time, the acute effect of decreasing urinary output is not sustained. The reason is that other factors, such as the arterial pressure, colloid osmotic pressure, and concentrations of the osmolar substances in the glomerular filtrate all change in the direction that leads eventually to a urinary volume output equal to the daily need.
- Aldosterone: This is secreted by the zona glomerulosa cells of the adrenal cortex by its action on the cells of the cortical collecting tubule to increase Na reabsorption and to increase K secretion.
- Angiotensin II: It increases Na and water reabsorption through following mechanisms:
[1] It stimulates aldosterone secretion, which in turn increases Na and water reabsorption. [2] It constricts the efferent arterioles and consequently increases Na and water reabsorption through the following mechanisms: [A]
When the angiotensin constricts the efferent arterioles, this reduces
the peritubular capillary pressure causing an increase in the rate of
reabsorption of water and electrolytes from the tubular system
especially from the proximal tubule, because the balance forces at the
capillary membrane is now in favor of absorption. [B] Because of
the constriction of the efferent arterioles, the blood flow through
glomeruli is decreased while the GFR is still near normal. This will
lead that a very high proportion of plasma fluid to filter through the
glomerular membrane into tubules. Therefore, the concentration of the
plasma proteins in the blood leaving the glomeruli becomes very high and
this concentrated plasma flows on into the peritubular capillaries. As
the result, the colloid osmotic pressure in these capillaries is greatly
increased, which is an additional factor that enhances reabsorption of
water and
salt.
[3] There is evidence that angiotensin also has a direct effect on the distal and proximal tubules in causing increased active reabsorption of Na and water by stimulating Na-K ATPase pump (at the basolateral membrane of the tubular cell) and Na-H exchange
(at the luminal side of the tubular
cell).
[4] Mesangial cells constrict in response to angiotensin
II and reduce the capillary filtration coefficient resulting in an
overall decrease in GFR. This reduction in GFR means less tubular fluid
flow and more Na and water reabsorption.
- Atrial natriuretic peptide: It is released from specific cells of the cardiac atria upon distension as a result of plasma volume expansion. It inhibits the reabsorption of Na and water by the renal tubules especially in the collecting ducts with consequent increase in the urinary output.
- Parathyroid hormone: It increases the reabsorption of Ca and Mg ions from the ascending limb of loop of Henle and distal tubule. It inhibits the reabsorption of phosphate from the proximal tubule.
- Nitric Oxide: When blood flow increases, a greater shear force acts on the endothelial cells in the arterioles and increases the production of NO. Increased production of NO causes dilation of the afferent and efferent arterioles in the kidneys.
Autoregulation of GFR (and renal blood flow):
It
is the feedback intrinsic mechanisms by which the kidneys normally keep
the renal blood flow (and consequently GFR) relatively constant,
despite marked changes in arterial blood pressure. GFR (125 ml/min) and
renal blood flow (1200 ml/min) normally they have to remain relatively
constant for both kidneys even the blood pressure changes from 80-200 mm
Hg.
There are specialized negative feedback mechanisms which
add together to provide the degree of GF and renal blood flow that is
required. These negative feedback mechanisms are:
[A] Tubuloglomerular feedback mechanism
[B] Myogenic mechanism
[A] Tubuloglomerular feedback mechanism: This occurs through JG complex.
[1] The afferent arteriolar vasodilator and vasoconstrictor
feedback mechanisms: A low GFR → decreases the ions concentration at
the macula densa → initiates a signal from the macula densa to the
juxtaglomerular cells → dilate the afferent arteriole →
increased blood flow into the glomerulus → increase in glomerular
pressure and hence GFR back toward the required level. And vice versa.
[2] The efferent arteriolar vasoconstrictor
feedback mechanism: Too few Na and Cl ions at the macula densa are
believed to cause JG cells to release renin and this in turn causes the
formation of angiotensin II which constricts mainly the efferent
arterioles (much more than the afferent arterioles). Therefore, the
constriction of the efferent arterioles causes the pressure in the
glomerulus to rise leading to increase in GFR back to normal. Renin is
an enzyme that release from renal juxtaglomerular cells and acts on a
substrate angiotensinogen. The cascade reaction is as shown in figure
below.
Renin release is increased if:
• Renal perfusion pressure is decreased,
• Renal blood flow is decreased,
• Stimulation of renal nerves.
[B] Myogenic mechanism:
This mechanism of stabilizing the GFR is based on the tendency of
smooth muscle to contract when stretched. When the arterial pressure
rises, it stretches the wall of the arteriole, and this in turn causes a
secondary contraction of the arteriole. This decreases the renal blood
flow and GFR back toward normal, thus opposing the effect of the rising
arterial pressure to increase the flow. Conversely, when the pressure
falls too low, an opposite myogenic response allows the artery to dilate
and therefore increases the flow and GFR.
Glomerulotubular
balance: It is the ability of the tubules to increase reabsorption rate in
response to increased tubular load, which means that when the GFR increases,
the rate of tubular reabsorption increases in exact proportion to the increase
in filtration. The mechanistic basis of glomerulotubular balance is
poorly understood. Glomerulotubular balance thus guarantees that the
majority of additional tubular flow, due to increases in GFR, is resorbed by
proximal segments of the nephron which are significantly more capable of
resorbing large fluid volumes. It should be pointed out that
glomerulotubular balance can be thought of as a second layer of protection
which follows mechanisms of Tubuloglomerular Feedback that attempt to maintain
nearly constant rates of GFR.
Tubular load of a substance: Is the total amount of the substance that filters through the glomerular membrane into tubules per minute.
Tubular
load = conc. of the substance in the filtrate x GFR. It is expressed in
gm/min. For example, if the plasma concentration of glucose is 100
mg/100 ml plasma, so the tubular load of glucose is equal to: 100 mg
glucose/100 ml plasma x 125 ml/min = 125 mg/min.
Renal handling of urea:
- At the proximal tubule: about 40% of the filtered urea is reabsorbed; however, because 60-80% of the filtered water is reabsorbed, the fluid leaving the proximal tubule has a urea concentration 2-3x that of plasma.
- At the thin loop of Henle: Somewhat permeable to urea. The high interstitial concentration of urea causes some of the interstitial urea to enter the lumen of the loop.
- At the thick ascending, distal tubule and cortical segment of the collecting duct: All are imperable to urea; as water is reabsorbed, urea becomes concentrated in the lumen.
- At the medullary collecting duct: Slightly permeable to urea, and this permeability is increased under the effect of ADH. As water is reabsorbed, the urea remaining within the duct becomes progressively more concentrated, which therefore diffuses out of the lumen into the interstitium in accordance with its concentration gradient
Which means 300 mOsmol/l at the cortex, about 800 mOsmol/l at the outer medulla, and as high as 1200-1400 mOsmol/l at the inner medulla. This gradient is due to:
- By the operation of the loops of Henle as countercurrent multipliers.
In general, a "countercurrent system" is a system in which the inflow runs parallel to, counter to (opposite to), and in close proximity to the outflow for some distance. This occurs for both the loop of Henle and the vasa recta of the renal medulla. The operation of each loop of Henle as a countercurrent multiplier depends on the following:
- Active transport of Na, K, Cl, and other ions out of thick ascending limb from the tubular lumen to the interstium. This pump able to create about 200 Mosmol concentration gradient between the interstial fluid and the tubular lumen.
- Diffusion of water by osmosis from the thin descending loop of Henle to the interstial fluid.
All of the above processes are essential to produce the increasing osmotic gradient along the medullar interstial fluid.
- By medullary interstitial urea concentration (Countercurrent concentration of urea, urea cycle) Urea contributes about 40-50% of the osmolarity of the renal medullary interstitium when kidney is forming maximally concentrated urine. Since the thick ascending limb of the loop of Henle, the distal convoluted tubule, and the cortical sections of the collecting duct are impermeable to urea, its concentration increases downstream in these parts of the nephron. ADH can make the inner medullary collecting duct more permeable to urea. Urea now diffuses back into the interstitium (where urea is responsible for about 40% of the high osmolality there) then transported back into the descending limb of the loop of Henle, comprising the recirculation of urea.
- By the operation of the vasa recta as countercurrent exchangers in addition to
- By the Slight medullar blood flow
[1] The Renal mechanism for excreting dilute urine
[2] The Renal mechanism for excreting concentrated urine
Na secretion:
The Kidneys adjust the final amount of Na that issue into the urine by [1] To reabsorb nearly all of it throughout the tubular system and [2] To adjust very carefully the remaining amount that is excreted for maintaining appropriate amounts of Na in the body fluids. This is achieved by
Na reabsorption in the distal tubule, cortical collecting tubule, and the collecting ducts which is controlled by aldosterone. In the presence of large amounts of aldosterone, almost the last amount of tubular Na are reabsorbed from these portions of the tubular system by active transport process coupled at least partially with active transport of K into the cells in opposite direction (i.e. K being exchanged for Na and therefore, none of Na enters the urine).
Potassium balance
External K+ homeostasis: Aldosterone is
the central hormone controlling K+ balance and produces effects on
both internal and external homeostasis. An increase in the extracellular fluid
[K+] stimulates aldosterone secretion directly. Consequently, cellular
uptake of K+ in skeletal muscle is increased, which reduces
extracellular fluid [K+], and renal K+ excretion is stimulated to
remove excess K+.
The Kidneys adjust the final amount of K+ that issue into the urine by [1] To reabsorb nearly all of it throughout the tubular system and [2] To adjust very carefully the remaining amount that is excreted for maintaining appropriate amounts of K+ in the body fluids. This is achieved by actively reabsorbed K+ in the distal tubules and cortical collecting tubules (via H-K ATPase countertransporter at the luminal membrane of tubular cells) which depend on the dietary K intake. Consequently, all the filtered K is actually reabsorbed back to the blood, which would eventually be lethal because of the toxic effects of K accumulation in the body. Therefore, active K secretion occurs in the principal cells in the late distal tubule and the cortical collecting duct (under the efect of aldosterone in an exchange to Na ions) is the principal means by which the tubular system controls the rate of K loss in the urine. This is occurs on a high K diet or high plasma K concentration.
On low K diet or low plasma K concentration, intracellular K decreases, so that the driving force for K secretion decreases. Also, the tubular α-intercalated cells are stimulated to reabsorb K by H-K ATPase.
In summary urinay K secretion is increased in:- High K diet
- High plasma K concentration
- Aldosterone excess
- Alkalosis
- Diuretics and diuresis
- High tubular Na
- Excess tubular anions
Renal regulation of extracellular fluid volume: The basic mechanism for fluid volume control is the
same as the basic mechanism for arterial pressure control. The renal role is
illustrated in the diagrams (figure 1 & figure 2).