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What are the effects of cortisol? Finish Adrenal glands cortisol Adrenal medulla & catecholamines Thyroid Gland • Thyroid Hormones • Calcium regulation 1. Energy Mobilization: a. ↑ glucose production by liver b. ↑ protein breakdown in muscle c. ↑ fatty acids in blood 2. Permissiveness a. Most other hormones work better in the presence of cortisol 3. Anti-inflammatory Adrenal Gland Part 2 Adrenal Medulla Hormone Zona glomerulosa • Recall cortisol is a lipid-soluble hormone aldosterone – Nuclear receptor activates transcription Cortex – e.g. cortisol ↑ tyrosine aminotransferase transcription, an enzyme important for glucose production in the liver Zona fasciculata Cortisol and Testosterone, progesterone Zona reticularis Medulla Epinephrine & norepinephrine Cortex Medulla 1 Adrenal Gland Part 2 Adrenal Medulla • Catecholamines stored in large vesicles within chromaffin cells of the adrenal medulla • Chromaffin cells innervated by neurons of the sympathetic nervous system • ‘Fight or flight’ response Sympathetic nerve terminal Acetycholine synapse Ca++ Adrenal medulla Catecholamine containing vesicles Chromaffin cell Blood vessel • Ach depolarizes chromaffin cell by activating nicotinic Ach receptors • Opens voltage-gated Ca++ channels • Ca++ causes fusion of vesicles • Release of catecholamine into blood stream Epi NE • Catecholamines released by adrenal medulla: – 80% epinipherine – 20% norepiniphrine Recall Norepinephrine is the Sympathetic NS postganglionic neurotransmitter 2 Effects of catecholamines depend upon receptor type • Activate adrenergic receptors Overall, Epi or NE from adrenal medulla have similar effects as NE from SNS activity – Two types: α and β • α2 α1 activates β1 β2 Phospholipase C Adenylate cyclase IP3 & DAG cAMP • • Effects Epi/NE from adrenal medulla last 5-10X longer than effects of SNS due to blood circulation Epi is a little more effective at activating β receptors than norepi Epi is more effective at ↑ metabolic rate of all cells inhibits Summary Thyroid • Pituitary gland – Hypothalamic control – Anterior – 2 hormone system – Posterior – direct hormone release into blood stream • Adrenal gland – Cortex – steroid hormones – Medulla - catecholamines 3 Thyroid • Thyroid Hormones – Produced in the follicle cells of the thyroid – T3 triiodothyronine – T4 thyroxine Follicular Cells • Both require iodine to be produced • Thyroid hormones increase metabolic rate in muscle, heart, liver and kidney – Produce heat Thyroid Follicle Follicle Cell Thyroid Follicle Thyroid hormone chemistry 30-fold concentration of iodide Iblood Thyroid peroxidase II- Na+ Na+ K+ T3 Formation and secretion of thyroglobulin in vesicles + tyrosine Thyroid peroxidase Monoiodotyrosine + I- diiodotyrosine Thyroglobulin + iodide monoiodotyrosine + diiodotyrosine = 3,5,3 triiodotyrosine (T3) endocytosis Thyroglobulin + T3 and T4 diiodotyrosine + diiodotyrosine = thyroxine (T4) proteolysis of thyroglobulin Release of T3 and T4 T4 4 What does TSH do on the follicle cell? Control of Thyroid Cold If –’ve feedback lost Too much TSH Get goiter Hypothalamic neurons TSH Rs Adenylate Cyclase Gs Thyroid releasing hormone (TRH) stimulates ATP Anterior Pituitary cAMP Thyroid Stimulating Hormone (TSH) Protein Kinase A Thyroid Actions of thyroid hormone T3, T4 lipid soluble → nuclear receptor T3 is 3X more active than T4 In target tissues T4 → T3 TH has many effects on just about all tissues Likely, 100s of enzymes ↑↑ in response to TH Some TH responsive genes include: • Glucose transporters (glut1) • Na+,K+ ATPase Increased breakdown of thyroglobulin Increased activity of iodide pump Increased rate of Tyrosine iodination Actions of thyroid hormone 1. ↑ In metabolic rate Basal Metabolic rate Release of thyroid hormones – T3 and T4 Thyroid hormone μg/day 2. ↑ responsiveness of β adrenergic receptors (esp. heart and nervous system) → excess thyroid hormone resembles excess sympathetic nervous system activity 5 Actions of thyroid hormone Growth & Development • General growth rate • Specific effects on nervous system, esp myelin production • Lack of iodine during development →Stunted growth, called cretinism Control of extracellular Calcium Tissues 1. Bone – 99% of total body calcium – Osteoblasts produce bone – Osteoclasts resorb bone Clinical →Enlargement of the thyroid, called goiter →Due to lack of thyroid hormones and overstimulation of the thyroid gland by TSH →Because no negative feedback Control of extracellular Calcium • Hormonal Control 1. Parathyroid hormone (PTH) 2. Calcitriol (1,25 dihydroxyvitamin D) 3. Calcitonin 2. Kidney – Excretion of calcium 3. GI tract – Calcium absorption 6 How do parathyroid cells sense calcium? Parathyroid • Low blood Ca++ stimulates release of parathyroid hormones • Act to increase blood Ca++ by – ↑ Ca++ release from bone – ↑ Ca++ absorption in gut – ↑ Ca++ reabsorption in kidney • Calcium-sensing receptor – Parathyroid cells – G-protein coupled receptor couple to IP3 pathway • This is odd, because in almost all other cells, ↑ [Ca++] causes ↑ secretion, Ca++ -- Phospholipase C • In parathyroid cells, ↑ [Ca++] causes ↓ secretion IP3 ??? Ca++ PTH Intracellular Ca++ stores 7 Vitamin D Skin Diet 7-dehydrocholesterol sunlight 1,25-OH Vitamin D acts as a co-factor to ↑ transcription of a Ca++ channel in the intestinal epithelium Vitamin D3 Plasma Vitamin D Vitamin D Liver 25-OH Vitamin D GI tract 1,25-OH2 Vitamin D Ca++ Kidney 25-OH Vitamin D Parathyroid Hormone 1,25-OH2 Vitamin D transcription Ca++ Na+ Intestinal epithelial cell Plasma 1,25-OH2 Vitamin D Calcitonin • Produced in parafollicle cells of the thyroid gland (C-cells) • High Blood Ca++ stimulates release of calcitonin (also by a calcium-sensing receptor) • Act to decrease blood Ca++ by High Ca++ Calcitonin Mobilize Ca From Bone Low blood Ca++ ↑ Parathyroid hormone Reabsorb Ca In the kidney – ↓ Ca++ release from bone – ↓ Ca++ reabsorption in kidney ↑1,25 OH2 Vit D from kidney Increase absorption of Ca++ from intestine restore blood Ca++ 8