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1. M.Prasad Naidu MSc Medical Biochemistry, Ph.D.Research
Scholar
2. 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%)
3. Adrenal medullary hormones are the amines derived from
catechol called catecholamines. 3 catecholamines are secreted by
medulla 1. Adrenaline or epinephrine (3g/dl) 2. Noradrenaline or
norepinephrine (30) 3. Dopamine (3.5g/dl of plasma)
4. 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. 5. Entry of dopamine into granules of chromaffin cells. 6.
Hydroxylation of dopamine into norEP by the enzyme
dopaminehydroxylase. 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.
6. 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.
7. 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
8. 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 & adrenergic receptors.
Receptor Response Mode of axn 1 More for NEP>EP Activates
phosplolipase C & IP3 2 More for NEP>EP adenyl cyclase and
cAMP 1 Same for both activates the above 2 EP>NEP same as
above
9. They give more response to NEP > EP 1 receptors exert
their actions by activating the 2nd messenger inositol tri
phosphate (IP3) through phospholipase C. 2 receptors exert their
effects by adenyl cyclase and reducing intracellular cAMP.
10. 1 receptors have mostly same degree of response to both EP
and NEP. 2 receptors are larger than 1 receptors and show more
response to EP than NEP Both 1 2 receptors produce their axns by
activating adenyl cyclase through G proteins and increasing
intracellular cAMP
11. Effects on metabolism:(via & 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)
12. 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.
13. NEP causes constriction of blood vessels throughout the
body via - receptors. NEP is called generalVasoconstrictor. EP also
constriction of blood vessels. However EP causes dialation of blood
vessels in skeletal muscle, liver & heart via 2 receptors.
14. 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.
15. Effects on respiration:-(via 2 recptors) EP rate &
force of respiration. EP also causes bronchodialation. Effects on
skin (via & 2 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.
16. 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.
17. 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