Download Human Physiology Respiratory System

by Talib F. Abbas
 Urea contributes to the establishment of the osmotic
gradient in the medullary pyramids and to the ability
to form a concentrated urine in the collecting ducts.
Urea transport is mediated by urea transporters,
presumably by facilitated diffusion. There are at least
four isoforms of the transport protein UT-A in the
kidneys (UT-A1 to UT-A4); UT-B is found in
erythrocytes.
 a high-protein diet increases the ability of the kidneys
to concentrate the urine.
 The osmotic gradient in the medullary pyramids
would not last long if the Na+ and urea in the
interstitial spaces were removed by the circulation.
These solutes remain in the pyramids primarily
because the vasa recta operate as countercurrent
exchangers.
 the solutes tend to recirculate in the medulla and
water tends to bypass it, so that hypertonicity is
maintained. The water removed from the collecting
ducts in the pyramids is also removed by the vasa recta
and enters the general circulation.
 Nilesat swees role
 The presence of large quantities of unreabsorbed
solutes in the renal tubules causes an increase in urine
volume called osmotic diuresis.
 Therefore, they “hold water in the tubules.” In
addition, the concentration gradient against which
Na+ can be pumped out of the proximal tubules is
limited. Osmotic diuresis is produced by the
administration of compounds such as mannitol and
related polysaccharides that are filtered but not
reabsorbed.
 For example, in diabetes mellitus, if blood glucose is
high, glucose in the glomerular filtrate is high, thus
the glucose will remain in the tubules causing
polyuria. Osmotic diuresis can also be produced by the
infusion of large amounts of sodium chloride or urea.
 In order to quantitate the gain or loss of water by excretion
of a concentrated or dilute urine, the "free water
clearance"(CH2O) is sometimes calculated. This is the
difference between the urine volume and the clearance of
osmoles (COsm):
 where V• is the urine flow rate and UOsm and POsm the urine
and plasma osmolality, respectively. COsm is the amount of
water necessary to excrete the osmotic load in a urine that
is isotonic with plasma. Therefore, CH2O is negative when
the urine is hypertonic and positive when the urine is
hypotonic.
‫وضع االهوار ضمن التراث العالمي‬
The cells of the proximal and distal tubules secrete
hydrogen ions.
 Acidification also occurs in the collecting ducts. The
reaction that is primarily responsible for H+ secretion
in the proximal tubules is Na–H exchange. This is an
example of secondary active transport; extrusion of
Na+ from the cells into the interstitium by Na, K
ATPase lowers intracellular Na+, and this causes Na+
to enter the cell from the tubular lumen, with coupled
extrusion of H+. The H+ comes from intracellular
dissociation of H2CO3, and the HCO3– that is formed
diffuses into the interstitial fluid. Thus, for each H+
ion secreted, one Na+ ion and one HCO3– ion enter
the interstitial fluid.
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 catalyzes the formation of H2CO3, and drugs that inhibit
carbonic anhydrase depress both secretion of acid by the
proximal tubules and the reactions which depend on it.
 Reactions in the renal tubular cells produce NH4+ and
HCO3–. NH4+ is in equilibrium with NH3 and H+ in the
cells. Because the pK' of this reaction is 9.0, the ratio of
NH3 to NH4+ at pH 7.0 is 1:100. However, NH3 is lipidsoluble and diffuses across the cell membranes down its
concentration gradient into the interstitial fluid and
tubular urine. In the urine it reacts with H+ to form NH4+,
and the NH4+ remains in the urine.
 The principal reaction producing NH4+ in cells is
conversion of glutamine to glutamate. This reaction is
catalyzed by the enzyme glutaminase, which is
abundant in renal tubular cells. Glutamic
dehydrogenase catalyzes the conversion of glutamate
to α-ketoglutarate, with the production of more NH4+.
Subsequent metabolism of α-ketoglutarate utilizes
2H+, freeing 2HCO3–.
 Renal acid secretion is altered by changes in the
intracellular PCO2, K+ concentration, carbonic
anhydrase level, and adrenocortical hormone
concentration. When the PCO2 is high (respiratory
acidosis), more intracellular H2CO3 is available to
buffer the hydroxyl ions and acid secretion is enhanced,
whereas the reverse is true when the PCO2 falls. K+
depletion enhances secretion, apparently because the
loss of K+ causes intracellular acidosis even though the
plasma pH may be elevated. Conversely, K+ excess in the
cells inhibits acid secretion. When carbonic anhydrase is
inhibited, acid secretion is inhibited because the
formation of H2CO3 is decreased. Aldosterone and the
other adrenocortical steroids that enhance tubular
reabsorption of Na+ also increase the secretion of H+
and K+.
 Although the process of HCO3– reabsorption does not
actually involve transport of this ion into the tubular
cells, HCO3– reabsorption is proportional to the
amount filtered over a relatively wide range.
 When the plasma HCO3– concentration is low, all the
filtered HCO3– is reabsorbed; but when the plasma
HCO3– concentration is high; that is, above 26 to 28
mEq/L (the renal threshold for HCO3–), HCO3–
appears in the urine and the urine becomes alkaline.
 when the plasma HCO3– falls below about 26 mEq/L,
the value at which all the secreted H+ is being used to
reabsorb HCO3–, more H+ becomes available to
combine with other buffer anions.
 Therefore, the lower the plasma HCO3– concentration
drops, the more acidic the urine becomes and the
greater its NH4+ content.
 Defense of H+ concentration: The mystique that
envelopes the subject of acid–base balance makes it
necessary to point out that the core of the problem is
not “buffer base” or “fixed cation” or the like, but
simply the maintenance of the H+ concentration of
the ECF.
 The rise in blood pressure produced by injection of
kidney extracts is due to renin, an acid protease
secreted by the kidneys into the bloodstream.
 This enzyme acts in concert with angiotensinconverting enzyme to form angiotensin II.
 plasma renin concentration (PRC): exogenous
angiotensinogen is often added, Deficiency of
angiotensinogen as well as renin can cause low plasma
renin activity (PRA) .
 The plasma angiotensin II concentration in such
subjects is about 25 pg/mL (approximately 25 pmol/L).
‫مؤتمر باريس لفتح الحصار ‪2005‬‬
 The renin in kidney extracts and the bloodstream is
produced by the juxtaglomerular cells (JG cells).
These epitheloid cells are located in the media of the
afferent arterioles as they enter the glomeruli.
 The membrane-lined secretory granules in them have
been shown to contain renin.
 Renin is also found in agranular lacis cells that are
located in the junction between the afferent and
efferent arterioles, but its significance in this location
is unknown.
 The lacis cells, the JG cells, and the macula densa
constitute the juxtaglomerular apparatus.
 intrarenal baroreceptor mechanism that causes renin
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secretion to decrease when arteriolar pressure at the
level of the JG cells increases.
Renin secretion is inversely proportional to the
amount of Na+ and Cl– entering the distal renal
tubules from the loop of Henle.
NO and K+ level effect the Renin secreation.
Angiotensin II feeds back to inhibit renin secretion by
a direct action on the JG cells.
Vassopressin inhibit renin.
increased activity of the sympathetic nervous system
increases renin secretion
‫بناء حمام تحت االرض في النجف مع ساللم ضمن برنامج خاليا السيس‬