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M.Prasad Naidu
MSc Medical Biochemistry,
Ph.D.Research Scholar
 Medulla is the inner part
 Forms about 20%
 It is made up of interlacing cords of cells, which contain
fine granules.
 granules are stained brown by K2Cr2O7
 These cells are called chromophil cells or pheochrom
cells or chromaffin cells.
 Chromaffin cells are of 2 types
 1.Adrenaline secreting cells (90%)
 2. Noradrenaline secreting cells (10%)
 Adrenal medullary hormones are the amines
derived from catechol called catecholamines.
 3 catecholamines are secreted by medulla
 1. Adrenaline or epinephrine (3µg/dl)
 2. Noradrenaline or norepinephrine (30)
 3. Dopamine (3.5µg/dl of plasma)
 CCA are syn fromTyr in the chromaffin cells of A.medulla.
 Various stages in the syn of CCAs:-
 1. Formation ofTyr from Phe in the presence of the enzyme
Phe.hydroxylase
 2. Uptake ofTyr from blood into the chromaffin cells of A.medulla by
ActiveTpt
 3. Convrsion ofTyr into dihydroxyphenylala (DOPA) by hydroxylation
in the presence ofTyrhydroxylase.
 4. Decarboxylation of DOPA into dopamine by DOPA decarboxylase.
 5. Entry of dopamine into granules of chromaffin cells.
 6. Hydroxylation of dopamine into norEP by the enzyme
dopamineβhydroxylase.
 7. Release of NEP from granules into the cytoplasm.
 8. Methylation of NEP into adrenaline by
phenylethenolamine-N-methyltransferase(PNMT
 PNMT is present in chromaffin cells.
 Half life of CCAs is about 2 minutes.
 85% of NEP is taken up by the sympathetic adrenergic neurons.
 The biological inactivation (degradation) and removal or remaining
15% of NEP and adrenal occurs as follows:
 1. EP is methylated into meta-adrenaline. NEP is methoxylated into
meta-noradrenalin .The methoxylation occurs in the presence of
Catechol-O-Methyltransferase (COMT)
 Meta-adrenaline and meta-noradrenaline are together called
metanephrines.
 2.Then, oxidation of metanephrines into
vanilylmandelic acid (VMA) occurs by
Monoamineoxidase (MAO)
 3. CCAs are removed from body through
urine in 3 forms.
 i) 50% as free or conjugated meta-adrenaline
and meta- noradrenaline
 ii) 35% asVMA and
 iii) 15% as free EP and free NEP
 The actions of EP and
NEP are excerted
through some receptors
(adrenergic receptors)
present in the target
organs.
 There are 2 types of
receptors called α&β
adrenergic receptors.
Receptor Response Mode of axn
α1 More for
NEP>EP
Activates
phosplolipase C
& IP3
Α2 More for
NEP>EP
↓adenyl cyclase
and cAMP
Β1 Same for
both
↑activates the
above
β2 EP>NEP same as
above
 They give more response to NEP > EP
 α1 receptors exert their actions by activating
the 2nd messenger inositol tri phosphate (IP3)
through phospholipase C.
 α2 receptors exert their effects by ↓ adenyl
cyclase and reducing intracellular cAMP.
 β1 receptors have mostly same degree of
response to both EP and NEP.
 β2 receptors are larger than β1 receptors and
show more response to EP than NEP
 Both β1 β2 receptors produce their axns by
activating adenyl cyclase through G proteins
and increasing intracellular cAMP
 Effects on metabolism:(via α&β receptors): EP
influences the metabolic functions more than NEP.
 1.General Metabolism:- i) ↑ O2
consumption and CO2 removal.
 It ↑ BMR.
 It is said to be calorigenic hormone.
 ii) Carbohydrate metabolism:- EP ↑ blood glucose
level.(↑ glycogenolysis in liver and mus)
 iii)fat metabolism:- ↑ lipolysis in AT ( for this function
Cortisol need the presence of Cortisol)
 Adrenaline ↓ blood clotting time.
 It ↑ RBC count and Hb content in blood by causing
contraction of spleen and release of RBC into
circulation.
 Effects on Heart:- EP has stronger effects on heart than
NEP.
 It ↑ the overall activity of Heart.i.e. rate (chronotropic
effect) , force of contraction (inotropic effect) and
excitability of muscle.
 NEP causes constriction of blood vessels
throughout the body via α- receptors.
 NEP is called generalVasoconstrictor.
 EP also  constriction of blood vessels.
 However EP causes dialation of blood vessels
in skeletal muscle, liver & heart via β2
receptors.
 EP ↑ systolic blood pressure by ↑ the force of
contraction and cardiac output.
 But it ↓ diastolic pressure by reducing the total
peripheral resistance.
 NEP ↑ diastolic pressure due to general vasoconstrictor
effect by ↑ the total peripheral resistance.
 It also ↑ the systolic blood pressure by the actions of
heart.
 Hypersecretion develops in excessive secretion of
catecholamines.
 Effects on respiration:-(via β2 recptors)
 EP ↑ rate & force of respiration.
 EP also causes bronchodialation.
 Effects on skin (via α & β2 receptors):-
 EP ↑ secretion of sweat.
 Effects on skeletal muscle:-
 EP causes severe contraction & quick fatigue of skeletal
muscle.
 It ↑ glycogenolysis and release glu into blood.
 It also causes vasodialation in skeletal muscles.
 Effects on Central Nervous system:-
 EP ↑ the activity of brain.
 Release of EP ↑ during fight or flight reactions after
exposure to stress.
 Other physiological functions:-
 1.CCAs cause vasoconstriction in salivary glands leading
to mild ↑ in salivary secre
 2. CCAs also ↑ the secretary activity of lacrimal glands.
 3. EP ↑ the release of ACTH.
 During stress conditions, a large quantity of
CCAs is secreted.
 During rest, a small quantity of CCAs is
secreted.
 These hormones prepare the body for fight or
flight reactions.
 CCAs secretion is also ↑ in conditions like
 1. Exposure to cold
 2. hypoglycemia

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A.medulla

  • 1. M.Prasad Naidu MSc Medical Biochemistry, Ph.D.Research Scholar
  • 2.
  • 3.  Medulla is the inner part  Forms about 20%  It is made up of interlacing cords of cells, which contain fine granules.  granules are stained brown by K2Cr2O7  These cells are called chromophil cells or pheochrom cells or chromaffin cells.  Chromaffin cells are of 2 types  1.Adrenaline secreting cells (90%)  2. Noradrenaline secreting cells (10%)
  • 4.  Adrenal medullary hormones are the amines derived from catechol called catecholamines.  3 catecholamines are secreted by medulla  1. Adrenaline or epinephrine (3µg/dl)  2. Noradrenaline or norepinephrine (30)  3. Dopamine (3.5µg/dl of plasma)
  • 5.  CCA are syn fromTyr in the chromaffin cells of A.medulla.  Various stages in the syn of CCAs:-  1. Formation ofTyr from Phe in the presence of the enzyme Phe.hydroxylase  2. Uptake ofTyr from blood into the chromaffin cells of A.medulla by ActiveTpt  3. Convrsion ofTyr into dihydroxyphenylala (DOPA) by hydroxylation in the presence ofTyrhydroxylase.  4. Decarboxylation of DOPA into dopamine by DOPA decarboxylase.
  • 6.  5. Entry of dopamine into granules of chromaffin cells.  6. Hydroxylation of dopamine into norEP by the enzyme dopamineβhydroxylase.  7. Release of NEP from granules into the cytoplasm.  8. Methylation of NEP into adrenaline by phenylethenolamine-N-methyltransferase(PNMT  PNMT is present in chromaffin cells.
  • 7.  Half life of CCAs is about 2 minutes.  85% of NEP is taken up by the sympathetic adrenergic neurons.  The biological inactivation (degradation) and removal or remaining 15% of NEP and adrenal occurs as follows:  1. EP is methylated into meta-adrenaline. NEP is methoxylated into meta-noradrenalin .The methoxylation occurs in the presence of Catechol-O-Methyltransferase (COMT)  Meta-adrenaline and meta-noradrenaline are together called metanephrines.
  • 8.  2.Then, oxidation of metanephrines into vanilylmandelic acid (VMA) occurs by Monoamineoxidase (MAO)  3. CCAs are removed from body through urine in 3 forms.  i) 50% as free or conjugated meta-adrenaline and meta- noradrenaline  ii) 35% asVMA and  iii) 15% as free EP and free NEP
  • 9.  The actions of EP and NEP are excerted through some receptors (adrenergic receptors) present in the target organs.  There are 2 types of receptors called α&β adrenergic receptors. Receptor Response Mode of axn α1 More for NEP>EP Activates phosplolipase C & IP3 Α2 More for NEP>EP ↓adenyl cyclase and cAMP Β1 Same for both ↑activates the above β2 EP>NEP same as above
  • 10.  They give more response to NEP > EP  α1 receptors exert their actions by activating the 2nd messenger inositol tri phosphate (IP3) through phospholipase C.  α2 receptors exert their effects by ↓ adenyl cyclase and reducing intracellular cAMP.
  • 11.  β1 receptors have mostly same degree of response to both EP and NEP.  β2 receptors are larger than β1 receptors and show more response to EP than NEP  Both β1 β2 receptors produce their axns by activating adenyl cyclase through G proteins and increasing intracellular cAMP
  • 12.  Effects on metabolism:(via α&β receptors): EP influences the metabolic functions more than NEP.  1.General Metabolism:- i) ↑ O2 consumption and CO2 removal.  It ↑ BMR.  It is said to be calorigenic hormone.  ii) Carbohydrate metabolism:- EP ↑ blood glucose level.(↑ glycogenolysis in liver and mus)  iii)fat metabolism:- ↑ lipolysis in AT ( for this function Cortisol need the presence of Cortisol)
  • 13.  Adrenaline ↓ blood clotting time.  It ↑ RBC count and Hb content in blood by causing contraction of spleen and release of RBC into circulation.  Effects on Heart:- EP has stronger effects on heart than NEP.  It ↑ the overall activity of Heart.i.e. rate (chronotropic effect) , force of contraction (inotropic effect) and excitability of muscle.
  • 14.  NEP causes constriction of blood vessels throughout the body via α- receptors.  NEP is called generalVasoconstrictor.  EP also  constriction of blood vessels.  However EP causes dialation of blood vessels in skeletal muscle, liver & heart via β2 receptors.
  • 15.  EP ↑ systolic blood pressure by ↑ the force of contraction and cardiac output.  But it ↓ diastolic pressure by reducing the total peripheral resistance.  NEP ↑ diastolic pressure due to general vasoconstrictor effect by ↑ the total peripheral resistance.  It also ↑ the systolic blood pressure by the actions of heart.  Hypersecretion develops in excessive secretion of catecholamines.
  • 16.  Effects on respiration:-(via β2 recptors)  EP ↑ rate & force of respiration.  EP also causes bronchodialation.  Effects on skin (via α & β2 receptors):-  EP ↑ secretion of sweat.  Effects on skeletal muscle:-  EP causes severe contraction & quick fatigue of skeletal muscle.  It ↑ glycogenolysis and release glu into blood.  It also causes vasodialation in skeletal muscles.
  • 17.  Effects on Central Nervous system:-  EP ↑ the activity of brain.  Release of EP ↑ during fight or flight reactions after exposure to stress.  Other physiological functions:-  1.CCAs cause vasoconstriction in salivary glands leading to mild ↑ in salivary secre  2. CCAs also ↑ the secretary activity of lacrimal glands.  3. EP ↑ the release of ACTH.
  • 18.  During stress conditions, a large quantity of CCAs is secreted.  During rest, a small quantity of CCAs is secreted.  These hormones prepare the body for fight or flight reactions.  CCAs secretion is also ↑ in conditions like  1. Exposure to cold  2. hypoglycemia