The h0rmones of adrenal medulla. University of Debrecen, Department of Physiology

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1 The h0rmones of adrenal medulla University of Debrecen, Department of Physiology

2 Introduction Adrenal gland (6-10 g) Cortex (5-9 g) Medulla ( 1 g) Chromaffin cells alarm (Selye 1936) flight or fight (Cannon 1929)

3 HO The hormones of the adrenal medulla HO HO catecholamines OH HO CH CH 2 NH CH 3 OH CH CH 2 NH 2 epinephrine All amount of epinephrine release from the adrenal medulla norepinephrine Small part of norepinephrine release from the adrenal medulla, the other part release from the sympathetic postganglionic fibre HO CH CH 2 NH 2 dopamine HO

4 Biosynthesis of catecholamines Rate limiting enzyme: activated by phosphorylation present in all sympathically activated tissues Regulation of biosynthesis: NH2 HC CH2 COOH Fenilalanin hidroxiláz NH2 HC CH2 COOH tirozin- hidroxiláz NH2 HC acut regulation: COOH CH2 Catalytic activity of tyrosine Hydroxylase (substrate, cofactors, end-product inhibition) NH PNMT CH3 OH Dopamin β-hidroxiláz NH2 HO OH long-term regulation: DOPA Dekarboxiláz NH2 Alterations in enzyme concentration HC OH HC OH CH2 CH2 CH2 PNMT: feniletanolamin N-metiltranszferáz CH2 cortisol influences the PNMT activity HO HO HO

5 Storage and release Sympathetic fibre Voltage-gated Ca 2+ channel Content of cromaffin granules: catecholamines (80% epinephrine, 20% norepinephrine) adrenomedullin opioid peptides dopamin β-hydroxylase ATP (ATP/catecolamine=1/4) the hormones and neurotransmitters neuropeptid Y nachr Na + secretion Ca 2+ transcription nucleus

6 Metabolism Half-time of catecholamine is about 2 min 50 % of circulating catecholamines are bound to proteins Reuptake into the axon terminals Dilution by diffusion out of junctional cleft degradation Catecholamines entered the circulation inactivated initially by COMT Catecholamines is released intraneuronally is inactivated initially by MAO sulfotransferases 1% of hormones is excreted by urine Plazma E/NE=1/7 instead 4/1!! epinephrine norepinephrine MAO COMT COMT MAO Mandelic acid (VMA) MAO (monoamin-oxidase; located within mitochondrium) COMT (katekol O'-metiltransferase; located in cytoplasm) Konjugated product

7 Autonomic Nervous System Sympathetic fibre Parasyimpathetic fibre Neurotransmitter Receptor Preganglionic fibre: ACh nachr Postganglionic fibre: NE, E, AR ganglion ganglion Epinephrine=adrenaline Norepinephrine=noradrenaline Neurotransmitter Receptor Preganglionic fibre: ACh nachr Postganglionic fibre: ACh machr

8 Factors resulting increased adrenomedullar secretion trauma, pain danger, fear, excitement hypotension, anoxia hypothermia, hypoglycemia Intense exercise

9 Circulating concentrations of catecholamines Plasma epinephrine Plasma norepinephrine basal 1x 1x Upright position 2x 2x Moderate excercise 3x 5x Hypoglycaemia 25x 1x Diabetes 15x 5x

10 Differences between sympathetic activation and stimulation of adrenal medulla Sympathetic activation Some organs, tissue has no innervation Immediate effects Rapid decay when activation is over Lokalized effects Adrenal stimulation Excert its effects in all cells Delay in the beginning Prolonged effects (3-5 min) Only generalized effects The dual mechanism of sympathetic stimulation provides a safety factor and either can substitute the other in most instances.

11 Catecholamine receptors PLC 1 : 1A, 1B, 1D G q -protein PLA 2 PLD Adrenoceptor 2 : 2A, 2B, 2C G i -protein Adenilát -cikláz 1 camp 2 G S -protein Adenilát -cikláz 3 ATP

12 Distribution of catecholamine receptors 1 : selective agonist: Phenylephrin selective antagonist: Prazosin, Phenoxybenzamin - Vascular smooth muscle (arteris and veins) contraction - Genitourinary smooth muscle contraction - Intestinal smooth muscle relaxation α 2 camp α 2 α 1 2 : selective agonist : Clonidin selective antagonist:yohimbin camp IP 3 Presynaptic sites - neural membranes, mediates inhibition of neurotransmitter release Postsinaptic sites - islet cells decreased insulin secretion - vascular smooth muscle contraction (more 2 receptors are located in the venous system than in arteries)

13 Distribution of catecholamine receptors 1 -receptors: 2 -receptors: selective agonist:albuterol selective antagonist: Butoxamine - Smooth muscle (vascular, brochial, GI, genitourinary) relaxation - liver glycogenolysis, gluconeogenesis - Skeletal muscle glykogenolysis, K + uptake 3 -receptors: selective agonist: Dobutamine selective antagonist: Metoprolol - myocardium positive inotropic, chronotropic, dromotropic, bathmotropic, lusitropic effects - JGA increased renin secretion -adipose tissue lipolysis Affinity of catecholamines to receptors Adrenalin: > Noradrenalin: <

14 Effects of circulating epinephrine: Low dose of epinephrine MAP ~ CO TPR ~ EDV SV ESV (+ inotropy) Heart rate viscosity Blood vessel diameter Increased heart rate and positive inotropy ß 1 Vasoconstriction in most systemic arteries and veins 1 and 2 (postsynaptic) Vasodilatation in muscle and liver vasculatures β 2 MAP = mean arterial pressure, CO = cardiac output, SV = stroke volume TPR = total peripherial resistance, EDV = end diastolic volume ESV = end systolic volume Effects of circulating epinephrine: CO MAP TPR High concentration of epinephrine EDV SV ESV (+ inotropy) Heart rate then viscosity Blood vessel diameter Positive ionotropy ß 1 Vasoconstriction in most systemic arteries and veins 1 and 2 (postsinaptic) Vasoconstriction in muscle and liver vasculatures 1

15 Effects of norepinephrine: CO ~ MAP TPR EDV SV ESV (+ inotropy) Heart rate then viscosity Blood vessel diameter Positive inotropy ß 1 Vasoconstriction in most systemic arteries and veins 1 and 2 (postsynaptic) Vasodilatation in coronaries indirect effect or ß 2 MAP = mean arterial pressure, CO = cardiac output, SV = stroke volume TPR = total peripherial resistance, EDV = end diastolic volume ESV = end systolic volume

16 Physiological effects of catecholamines epinephrine Norepinephrine ( ) ( ) P systole P diastole ~ MAP SV ~ CO ~ Heart rate (reflex) Blood flow TPR ~ coronaries MAP CO TPR SV Heart rate EDV ESV Blood vessel diameter viscosity HR P S MAP P D CO TPR

17 Physiological effects of catecholamines Visceral smooth muscle Relaxation is mediated by β 2 receptors Contraction is mediated by α 1 receptors Epinephrine Norepinephrine GI tract smooth muscle tone (α 2 ) amplitudes of contractions (α 2 ) sphincter contraction contraction Uterus pregnant relaxation contraction nonpregnant contraction penis & seminal vesicule ejaculation Urine bladder detrusor muscle relaxation relaxation (α 2 ) trigone muscle contraction contraction Bronchiolar smooth muscle relaxation

18 Metabolic effects of epinephrine hyperglycemia (α and β receptors) hyperlactacidaemia hyperlipidaemia (FFA ) Plasma amino acido level O 2 consumption Basal metabolic rate (~15-30 %) Fall in plasma K + ( stimulation of K + uptake into cells, due β 2 receptor activation) 1. Liver Glycogenolysis Gluconeogenesis Glycogen synthesis 2. Pancreatic islet cells Insulin secretion (α) Glucagon secretion (β) 3. Skeletal muscle Glycogenolysis Glucose uptake Lactate production Proteolysis 4. Adipose tissue Lipolysis (β 3 )

19 Physiological effects of catecholamines Effects on the secretion of the other hormones The effect of epinephrine is rather short-term than long-term regulation on other hormones Sympathetic stimulation or catecholamines Renin secretion Pancreatic islet - insulin secretion (α) - glucagon secretion (β) Thyroid hormone synthesis and release (α) Growth hormone secretion (α)

20 Effects of catecholamines -effect Epinephrine > Norepinephrine liver: Glycogenolysis Adipose tissue: Lipolysis Pancreatic islet : Insulin secretion Pancreatic islet : Glucagon secretion heart: contractility heart: relaxation heart: heart rate Vascular vasodilatation (coronary, skeletal muscle) Muscle relaxation: GI Urine bladder Bronchiolar Pregnant Uterus -effect Epinephrine < Norepinephrine Liver: Gluconeogenesis Pancreatic islet: Insulin secretion Heart: hypertrophy Vascular vasoconstriction (liver, kidney) Sphincter contraction

21 Stress Short-term stress response Effects of epinephrine 1.Glycogen broken down to glucose - increased blood glucose 2. Increased blood pressure 3. Increased breathing rate 4. Increased metabolic rate 5. Change in blood flow patterns, leading to increased alertness and decreased digestive and kidney activity Long-term stress response Effects of mineralocorticoids 1. Retention of sodium ions and water by kidney 2. Increased blood volume and blood pressure Effects of glucocorticoids 1. Proteins and fats broken down and converted to glucose, leading to increased blood glucose 2. Immune system may be suppressed

22 Disadvantages of repeated and prolonged stress production of anabolic steroids (inhibition of GH, TRH, GnRH secretion and T4 T3 conversion) Cardiovascular effects: MAP, hyperlipidemia Suppression of immune function Reduced number of cells in the hippocampus (the brain`s primary memory center) memory loss and impaired learning (long-term exposure to CRF and cortisol) Epinephrine and cortisol work together to create memories of emotional events. It seems that an event that felt so emotionally charged burned forever into your memory. Blood sugar levels increase elevated insulin production `burnout` of pancreas Loss of calcium from bones

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