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Lecture 4

Lecture 4 Calcium balance.doc

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Department
Physiology
Course
PSL300H1
Professor
Michelle French
Semester
Fall

Description
Lecture 4: Calcium balance October-24-12 10:04 PM Ca is critical for normal physiology • Intracellular signalling • Hormone secretion (triggers excoytosis) • Blood clotting • Neural excitability • Muscle contraction (permits actin and myocin interaction) • Building and maintaining bone • e.g. calcium triggers a reaction so that no other sperm can go into the oocyte Total body Ca2+ = intracellular +extracellular (ECF/plasma +bone) • Ca from diet -> small intestine absorbs into blood • Bone resorption = dissolving of bone • Small intestine -> (4 mmoles) -> ECF (1% Ca, [Ca2+] = 2.5 mM) • Bone (99% Ca) ECF • Kidney ECF, also, Kidney -> 4mmoles -> urine • Cells (.9 % Ca, [Ca2+] = .001mM) • Ca gained is the same amount lost in urine • Balance of Ca in body if not growing Bone is constantly being formed and resorbed • Calcium in bone is mainly in crystals (hydroxyapatite) a small fraction is ionized and readily exchangeable • Ca can go in or out through blood vessel and nerve • Bone made of spongy and compact bone - o Compact can withstand lots of direct force o Spongy bone can deal with lateral hits Cells responsible for bone growth/turnover • Osteoblast (bone forming) • Osteocyte (maintain matrix) - hydroxyapatite found here • Osteoclasts (bone resorption) - have extra nuclei because formed from the fusion of cells • Calcium turnover/year = 100% in infants, 18% in adults Osteoclasts • Secrete protons into sealed off areas • Breakdown of bones -> blood capillaries nearby so Ca and phosphate can go into the blood stream • Area of bone resorbtion • Good to have coordination between osteoclasts and osteoblasts Bone dynamics (~100 days): osteroclasts resorb, osteoblasts form, osteocytes (retired osteoblasts) 1. Resting phase 1. Resorption- osteoclasts break down lining cells of bone 2. Cavity made by osteoclasts 3. Formation and repair by osteoblasts (new bone formed) Osteoblasts promote osteoclast formaiton via RANKL/RANK interaction •Cell-cell communication between RANKL & RANK •RANKL (RANK- ligand, found on osteoblast) binds to RANK causing osteoclast precursors to differentiate and fuse •Interaction through membrane protein, local communication •RANK = receptor activator of nuclear factor kappa B (found on osteoclast precursor) •Osteoprotegrin (OPG) secreted by osteoblasts blocks RANKL/RANK interaction •OPG can bind to RANKL to block it •Kind of like negative feedback. Other hormones can also control Plasma Ca2+ level control •Done by parathyroid hormone (PTH), calcitriol (1,25-dihydroxycholecalciferol) and calcitonin •Act on 3 sites: bones, kidneys, digestive tract •PTH o Released from the parathyroid glands (chief cells) o Function: increase plasma Ca2+ concentration o Stimulus: low plasma Ca2+ o Parathyroid cells are very sensitive to changes in extracellular calcium concentration o The lower the [Ca2+], the more PH secreted • Switch happens very rapidl
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