1. © 2015 Pearson Education, Inc. Figure 18-14a The Adrenal Gland. A superficial view of the kidneys and adrenal glands a Right and left inferior phrenic arteries Left adrenal gland Left middle adrenal artery Left inferior adrenal arteries Left adrenal vein Left renal artery Left renal vein Superior mesenteric artery Abdominal aorta Inferior vena cava Right superior adrenal arteries Celiac trunk Right adrenal gland Right middle adrenal artery Right inferior adrenal artery Right renal artery Right renal vein p. 633

2. © 2015 Pearson Education, Inc. Figure 18-14b The Adrenal Gland. Cortex Medulla An adrenal gland in section b Capsule b p. 633

3. © 2012 Pearson Education, Inc. Figure 18-14c The Adrenal Gland Adrenal cortex Capsule Adrenal medulla Zona reticularis Zona fasciculata Zona glomerulosa Adrenal gland The major regions of an adrenal gland LM  140 p. 633 © 2015 Pearson Education, Inc.

4. Figure 18-14c The Adrenal Gland. The major regions and zones of an adrenal gland and the hormones they produce c Adrenal gland LM × 140 Region/ZoneHormonesPrimary Target Hormonal EffectsRegulatory Control The Adrenal Hormones ADRENAL CAPSULE ADRENAL CORTEX Zona glomerulosa Zona fasciculata Zona reticularis ADRENAL MEDULLA Mineralocorticoids, primarily aldosterone Glucocorticoids (cortisol [hydrocortisone], corticosterone) Androgens Epinephrine (E), norepinephrine (NE) Most cells Kidneys Increase renal reabsorption of Na + and water (especially in the presence of ADH), and accelerate urinary loss of K + Stimulated by angiotensin II, elevated blood K + or fall in blood Na + ; inhibited by ANP and BNP Stimulated by ACTH from the anterior lobe of the pituitary gland Increase rates of glucose and glycogen formation by the liver; release of amino acids from skeletal muscles, and lipids from adipose tissues; promote peripheral utilization of lipids; anti-inflammatory effects Androgen secretion is stimulated by ACTH. Adrenal androgens stimulate the development of pubic hair in boys and girls before puberty. Increases cardiac activity, blood pressure, glycogen breakdown, blood glucose levels; releases lipids by adipose tissue Stimulated by sympathetic preganglionic fibers p. 633

5. © 2015 Pearson Education, Inc. 18-10 Hormone Interactions The Hormonal Responses to Stress General Adaptation Syndrome (GAS) Also called stress response How body responds to stress-causing factors Is divided into three phases 1. Alarm phase 2. Resistance phase 3. Exhaustion phase p. 645

6. © 2015 Pearson Education, Inc. Figure 18-20 The General Adaptation Syndrome (Part 1 of 3). During the alarm phase, an immediate response to the stress occurs. The sympathetic division of the autonomic nervous system directs this response. In the alarm phase, (1) energy reserves are mobilized, mainly in the form of glucose, and (2) the body prepares to deal with the stress-causing factor by “fight or flight” responses. Epinephrine is the dominant hormone of the alarm phase. Its secretion is part of a generalized sympathetic activation. Brain Sympathetic stimulation Adrenal medulla General sympathetic activation Epinephrine, norepinephrine Alarm Phase (“Fight or Flight”) Immediate Short-Term Responses to Crises Increased mental alertnessIncreased energy use by all cellsMobilization of glycogen and lipid reservesChanges in circulationDecreased digestive activity and urine productionIncreased sweat gland secretionIncreased heart rate and respiratory rate p. 645

7. © 2015 Pearson Education, Inc. Figure 18-20 The General Adaptation Syndrome (Part 2 of 3). If a stress lasts longer than a few hours, the person enters the resistance phase of GAS. Glucocorticoids are the dominant hormones of the resistance phase. Epinephrine, GH, and thyroid hormones are also involved. Energy demands in the resistance phase remain higher than normal, due to the combined effects of these hormones. Neural tissue has a high demand for energy, and requires a reliable supply of glucose. If blood glucose levels fall too low, neural function deteriorates. Glycogen reserves can meet neural demand during the alarm phase, but become depleted after several hours. Hormones of the resistance phase mobilize lipids and amino acids as energy sources to conserve glucose for use by neural tissue. Growth hormone Resistance Phase Glucagon Pancreas Adrenal cortex ACTH Glucocorticoids Mineralocorticoids (with ADH) Sympathetic stimulation Kidney Renin-angiotensin- aldosterone system Long-Term Metabolic Adjustments Mobilization of remaining energy reserves: Lipids are released by adipose tissue; amino acids are released by skeletal muscleConservation of glucose: Peripheral tissues (except neural) break down lipids to obtain energyElevation of blood glucose concentrations: Liver synthesizes glucose from other carbohydrates, amino acids, and lipidsConservation of salts and water, loss of K + and H + p. 645

8. © 2015 Pearson Education, Inc. Figure 18-20 The General Adaptation Syndrome (Part 3 of 3). The body’s lipid reserves are sufficient to maintain the resistance phase for weeks or even months. But when the resistance phase ends, homeostatic regu- lation breaks down and the exhaustion phase begins. Unless corrective actions are taken almost immediately, the failure of one or more organ sys- tems will prove fatal. The production of aldosterone throughout the resistance phase results in a conservation of Na + at the expense of K +. As the body’s K + content decreases, a variety of cells begin to malfunction. The underlying problem of the exhaustion phase is the body’s inability to sustain the endocrine and metabolic adjustments of the resistance phase. Exhaustion Phase Collapse of Vital Systems Exhaustion of lipid reservesCumulative structural or functional damage to vital organsInability to produce glucocorticoidsFailure of electrolyte balance p. 645

9. © 2015 Pearson Education, Inc. Figure 18-16a The Pancreas. The gross anatomy of the pancreas Small intestine (duodenum) Head of pancreas Accessory pancreatic duct Common bile duct Pancreatic duct Body of pancreas Lobule Tail a p. 635

10. © 2015 Pearson Education, Inc. Figure 18-16b The Pancreas. A pancreatic islet surrounded by exocrine cells Pancreatic islet LM × 400 Capillary Pancreatic islet (islet of Langerhans) Pancreatic acini (clusters of exocrine cells) b LM × 400 p. 635

11. © 2015 Pearson Education, Inc. Figure 18-17 The Regulation of Blood Glucose Concentrations (Part 1 of 2). Increased rate of glucose transport into target cells Increased rate of glucose utilization and ATP generation Increased conversion of glucose to glycogen Increased amino acid absorption and protein synthesis Increased triglyceride synthesis in adipose tissue Blood glucose levels decrease HOMEOSTASIS RESTORED HOMEOSTASIS DISTURBED Beta cells secrete insulin Increasing blood glucose levels HOMEOSTASIS Normal blood glucose levels (70–110 mg/dL) p. 636

12. © 2015 Pearson Education, Inc. Figure 18-17 The Regulation of Blood Glucose Concentrations (Part 2 of 2). HOMEOSTASIS Normal blood glucose levels (70–110 mg/dL) Decreasing blood glucose levels Blood glucose levels increase HOMEOSTASIS RESTORED HOMEOSTASIS DISTURBED Alpha cells secrete glucagon Increased breakdown of glycogen to glucose (in liver, skeletal muscle) Increased breakdown of fat to fatty acids (in adipose tissue) Increased synthesis and release of glucose (by the liver) p. 636

13. Copyright © 2009 Pearson Education, Inc., publishing as Pearson Benjamin Cummings © 2012 Pearson Education, Inc. © 2015 Pearson Education, Inc. p. 636

14. © 2015 Pearson Education, Inc. Figure 18-19a Endocrine Functions of the Kidneys. Digestive tract Sunlight Epidermis Cholesterol Cholecalciferol PTH Intermediate form Parathyroid glands Dietary cholecalciferol Stimulation of calcium and phosphate ion absorption Kidney Calcitriol The production of calcitriol Liver a p. 641

15. © 2015 Pearson Education, Inc. Figure 18-19b Endocrine Functions of the Kidneys. HOMEOSTASIS HOMEOSTASIS DISTURBED Falling blood pressure and volume Kidney Normal blood pressure and volume Falling renal blood flow and O 2 Erythropoietin released Renin released HOMEOSTASIS RESTORED Rising blood pressure and volume Increased red blood cell production Increased fluid intake and retention Aldosterone secreted ADH secreted Stimulation of thirst ACE Angiotensin II Angiotensin I Angiotensinogen The release of renin and erythropoietin, and an overview of the renin- angiotensin-aldosterone system beginning with the activation of angiotensinogen by renin b p. 641