Urine formation, hormonal control

drmubasher 8,894 views 4 slides Mar 16, 2017
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M Phil lectures


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Urine Formation
Urine formation is eventually sum of three basic renal
process; the glomerulus filtration, tubular reabsorption and
tubular secretion.
Urinary Excretion = GF - TR + TS
GF (Glomerulus Filtration)
TR (Tubular Reabsorption of NaCl, H2O, PO4
---
and Ca
++
)
TS (Tubular secretion of H
+
and K
+
)
Hormonal control
The renal processes listed above are controlled by hormones
and sympathetic nervous system. Aldosterone, Angiotension
II, Antidiuretic hormone ADH, Atrial Natriuretic peptide and
parathyroid hormone controls the whole mechanism of urine
filtration, reabsorption and secretions.
Aldosterone
Secreted by zona granulose of adrenal cortex, regulates
sodium reabsorption and potassium secretion by renal
tubules. Primarily acts on principal cells of cortical collecting
tubules by activating sodium potassium ATPase pump on
basolateral side of cortical collecting tubules for the activity.
Thus it increases sodium permeability of luminal side of
tubular cell.
Absence of Aldosterone causes remarkable loss of Na+ and
accumulation of K++, the phenomenon termed into
Addison’s disease. Excessive Aldosterone causes sodium
retention and potassium depletion, the phenomenon is
termed as Conn’s syndrome (Adrenal tumors)
Angiotension II
This is most powerful sodium retaining hormone. It acts in
certain situations like low blood pressure and low extra
cellular fluid. It acts by increasing sodium and water
reabsorption from renal tubules to return blood pressure
and extracellular fluid to normal. The whole process is
followed by:
GENERAL PRINCIPLES OF PHYSIOLOGY
PHYS- 701

Topic
Urine formation
Hormonal
control
Mubasher Solangi
M.Phil (Pursuing)

Supervisor
Dr. Moolchand Malhi, PhD
Assistant Professor
Dept: of Physiology & Biochemistry
Faculty of A.H and Veterinary Sciences
SAU Tando Jam

pH
Activities of almost all enzyme
systems within body are influenced
by H
+
concentration. Substances that
release H
+
are referred as Acids and
substance that tendency to receive H
+

are referred to as Bases. H
+
is single
free proton released by hydrogen
atom.
Kidneys control acid-base balance by
secreting acidic or basic urine. HCO-
3 are filtered continuously in tubules,
if excreted into urine it removes base
from blood.



29/02/2016

Editor: Mubasher Solangi, M.Phil (Pursuing)
Supervisor: Dr. Mool Chand Malhi, PhD
General Principles of Physiology (PHYS-701)
Assignment | Urine formation, Hormonal control


2
Department of Physiology and Biochemistry, Faculty of Animal Husbandry and Veterinary Sciences
Sindh Agriculture University Tando Jam
 Stimulation of Aldosterone secretion
 Constriction of efferent arterioles
 Stimulation of sodium reabsorption
Stimulation of Aldosterone secretion
Aldosterone increases sodium permeability by activating sodium potassium ATPase pump at basolateral
surface of tubular cell thus permeability of sodium at luminal surface is increased. (Process discussed
earlier)
Constriction of efferent arterioles
Angiotension II causes efferent arteriole constriction which reduces peritubular hydrostatic pressure,
thus increasing net tubular reabsorption from proximal tubules. Second effect is by reducing renal blood
flow in efferent renal arteries which causes constriction. By reducing renal blood flow and rising
filtration rate in glomerulus, it increases protein concentration and colloid osmotic pressure in
peritubular capillaries. Thus reabsorption forces are increased at peritubular capillaries which rises
tubular reabsorption of sodium and water.
Stimulation of sodium reabsorption
Stimulation of sodium reabsorption in proximal tubules, loop oh Henle, distal tubules and collecting
tubules occurs by activation of sodium potassium ATPase pump at basolateral side of epithelial cell and
stimulation of sodium hydrogen exchange in luminal membrane, especially in proximal tubule. Thus
stimulate sodium transport across both luminal and basolateral surfaces.
Antidiuretic Hormone ADH (Vasopressin)
This hormone increases water permeability of distal tubule, collecting tubule of epithelia which helps
body to conserve water during dehydration. It binds with V2 receptors in late distal tubules, collecting
tubules and collecting ducts, increasing activity of cyclic AMP and activating protein kinesis. Binding with
V2 receptor causes movement of intracellular protein aquaporin 2 (AQP2) to the luminal side of cell
membrane where it forms a cluster of proteins and fuses with cell membrane by exocytosis. By the
process water channels are formed that permit rapid diffusion of water inside cell.
Some other proteins like AQP3 and AQP 4 are present at basolateral side of cell but they are not
controlled by ADH. These proteins provide a path to water to exit the cell.
By the action of ADH and transcription of AQP2 gene, a AQP2 protein is produced. Increase in ADH
causes rapid formation of AQP2 ultimately rapid movement of water inside cell occurs. While decreased
ADH causes reduced formation of AQP2 thus closure of water channels from luminal membrane occurs
and water permeability is reduced. In absence of ADH dilute urine is produces.

Editor: Mubasher Solangi, M.Phil (Pursuing)
Supervisor: Dr. Mool Chand Malhi, PhD
General Principles of Physiology (PHYS-701)
Assignment | Urine formation, Hormonal control


3
Department of Physiology and Biochemistry, Faculty of Animal Husbandry and Veterinary Sciences
Sindh Agriculture University Tando Jam

Neuroanatomy of the hypothalamus, where Antidiuretic hormone (ADH) is synthesized, and the
posterior pituitary gland from where ADH is released
Atrial Natriuretic Peptide
When plasma volume increases, specific cells of cardiac atria distended to secrete peptide called atrial
Natriuretic peptide. This is responsible for decrease in sodium and water reabsorption. Increase in
peptide causes inhabition of sodium and water thus increase in urine that helps to return blood volume
back towards normal.
Parathyroid hormone
This is one of the important calcium regulating hormones. It increases calcium reabsorption especially in
distal tubule and loop of henle. It also inhabits phosphate reabsorption by proximal tubules and
stimulates magnesium reabsorption by loop of henle.
Sympathetic Nervous System

Editor: Mubasher Solangi, M.Phil (Pursuing)
Supervisor: Dr. Mool Chand Malhi, PhD
General Principles of Physiology (PHYS-701)
Assignment | Urine formation, Hormonal control


4
Department of Physiology and Biochemistry, Faculty of Animal Husbandry and Veterinary Sciences
Sindh Agriculture University Tando Jam
Activation of sympathetic nervous system causes constriction of renal arterioles thus reducing sodium
and water reabsorption thereby reducing Glomerular Filtration Rate (GFR). It also increases sodium
absorption in proximal tubules, thick ascending limb of loop of henle and distal parts of renal tubules.
The sympathetic nervous system also responsible for rennin release and Angiotension II formation
which increases tubular reabsorption and decrease renal excretion of sodium.
Summary of hormones
Hormone Site of Action Effects
Aldosterone Collecting tubules and ducts Increase NaCl, H2O reabsorption
Increase K
+
secretion
Angiotension II Proximal Tubule, Thick ascending
loop of henle, distal tubule and
collecting ducts
Increase NaCl, H2O reabsorption
Increase H
+
secretion
Anti Diuretic Hormone (ADH) distal tubule, collecting tubules
and collecting ducts
Increase H2O reabsorption
Atrial Natriuretic Peptide distal tubule, collecting tubules
and collecting ducts
Decrease NaCl reabsorption
Parathyroid Hormone Proximal tubules, Thick ascending
loop of henle and distal tubule
Decrease PO4
---
reabsorption
Increase Ca
++
reabsorption



BIBLIOGRAPHY:
Title Text book of Medical Physiology, 11
th
ed.
Author Arthur C, M.D. Guyton and J.E. Hall
Publication Date 2006
Publisher SAUNDERS, An imprint of Elsevier
ISBN# 13: 978-07216-0240-0
10: 0-07216-0240-1

Title Text book of Animal Physiology
Author Lauralee Sherwood, Hillar Klandorf and paul H. Yancey
Publication Date 2008
Publisher Cengage Learning India Pvt. Ltd.
ISBN# 10: 81-315-1267-3
13: 978-81-315-1267-8