Published on March 27, 2014
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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