albi balqis
Post on 01-Jun-2015
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Ca 2+ homeostasis
Definition :
A maintainance/adjustment of constant free plasma [ca 2+ ] in our body.
Proportion of ca 2+
100% 1 %
0.9%
cell
0.1% ECF99%
bone 41% -plasma
protein
50% - free ions
9 % - anion
Functions of ca 2+
Blood clotting
Neuromuscular activity
Excitation-
contraction
coupling
Maintenance of tight junction btw cell
What is the effect if no ca
homeostasis??????
For example
↓ [ca 2+ ] in ECF
↓
↑ Na channel permeability
↓
More Na influx
↓
Easy reach threshold (even more negative value)
↓
Fire AP easily
↓
Spontaneous discharge of AP
Muscle cramp
For example
↑ [ca 2+ ] in ECF
↓
↓ Na channel permeability
↓
Less Na influx
↓
Difficult to reach threshold (even more negative value)
↓
Less AP
↓Muscle weakne
s
What are the factors can
alter [ ca 2+] in
ECF??
Alteration of the forms of Ca2+ in plasma
Changes in plasma protein
concentration-total
[ca]=[protein]-not cause parallel
change of ionized ca
↑[plasma protein]→↑total [ca]
↑[plasma protein]→↑t
otal [ca]
Changes in anion
concentration
alter the ionized Ca2+ concentration
↑[anion]→↑ ca complexed with anion→↓free ca
↑[anion]→↑ ca complexed with
anion→↓free ca
Acid-base abnormalities
alter the ionized Ca2+ concentration
Acidemia:↑H →↓ ca bind to
anion→↑ free ca
Alkalemia ; ↓ H→↑ca bind to anion→↓free ca
Regulatory mechanism
Calcium homeostasis involve 3 organs and 3 hormones
Kidney vitamin D
Intestine PTH [parathyroid hormone]
Bone calcitonin
To illustrate :
GIT- stimulated via vitamin D
we ingest 1000mg/dl
350mg/dl is absorbed from GIT
150mg/dl is secreted into GIT
Net absorption → 200mg/dl→ ca 2+ pool in ECF
Remaining 800mg/dl excreted into feces
Bone –stimulated by PTH + vit D and inhibit by calcitonin
Bone remodelling= bone resorption
No net gain or loss of ca
Kidney – stimulated by PTH
Approximately
10 %→excreted in urine
41% →ca bound to plasma protein
9 %→ combine with anion*
50 %→ ionized*
* filtered in the glomerulus
In renal tubules, 99 % is filtered
90 % - reabsorbed in proximal tubule,LOH,early distal tubule
9 % - is selective depending on ca 2+ concentration in blood
When [ca] ↓→reabsorption is great→almost no ca is lost in urine
When [ca] ↑→reabsorption is less→ ca is lost in urine
# the most important factor controlling this reabsorption in distal portion is PTH
calcitonin
Straight chain pepetide of 32
amino acid
Synthesize in parafollicular cell in thyroid
gland
Calcitonin receptor-
serpentine
Calcitonin have opposite effect to PTH.
Human bone
Not participate in minute-minute regulation of plasma ca in human
Main respond →inhibit osteolytic bone resorption
↓
↓ plasma ca
Calcitonin has weak effect on plasma ca in adult human
Why weak ?•Reduction ca by calcitonin lead to powerful stimulation of PTH which override calcitonin effect•In adult ,daily rate of reabsorbtion and deposition of ca are smaal compared to child or Paget disease (osteolytic activity is great and calcitonin effect is potent)
Immediate effect Prolonged effect
↑[ ca ] in plasma↓
Calcitonin stimulated to secrete
↓Calcitonin bind receptor
(coupled to G –protein )on osteoclast
↓Adenylyl
cyclase/phospholipase↓
• Inhibit resorption activity on osteoclast
↓↓ [ca] is released to ECF from
bone
Secondarily to ↓osteoclastic activity
↓formation of new osteoclast followed by decrease of osteoblast
↓activity of osteoclastic and osteoblastic activity
Pronounced effect of calcitonin on
• Paget disease
Increase osteoclastic activity→ calcitonin stimulation to inhibit resorption of bone→↓ [ca] in plasma
• pregnancy mother
Ca is needed for the formation of bone in infants and lactation process→ ca from mother’s bone→to prevent from excess resorption activity on bene→calcitonin action play its role
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