CoverModule 1.0. Homeostasis, Membranes, Electrophysiology and ANS1.1. Homeostasis1.1.1. Homeostasis Defined1.1.2. Homeostatic Control Systems1.1.3. Feedback Response Loop1.2. Cell Transport; Water & Solutes1.2.1. Fluid Compartments1.2.2. Osmosis1.2.3. Diffusion of Solutes1.2.4. Active Transport1.2.5. Bulk Transport1.3. Electrophysiology1.3.1. Ions and Cell Membranes1.3.2. Membrane Potentials1.3.3. Graded Potential1.3.4. Action Potentials1.3.5. Refractory Periods1.3.6. Propagation of an Action Potential1.4. The Synapse1.5. The Autonomic Nervous System1.5.1. Organization of the Nervous System1.5.2. Structural Organization of the ANS1.5.3. The SNS and the PNS1.5.4. The Enteric Nervous System1.5.5. Physiology of the ANS1.5.6. Neurotransmitters of the ANS1.5.7. Receptors of the ANS1.5.8. Actions of the Autonomic Nervous System1.5.9. Table of Actions for the SNS and PNS and Some Common DrugsModule 2.0. Skeletal Muscle and Special Senses2.1. Structural Organization of Skeletal Muscle2.2.1. Neuromuscular Junction, Excitation-Contraction Coupling2.2.2. Muscle Contractures and Cramps2.3. Whole Muscle Contraction, Fiber Type, Fatigue and Muscle Pharmacology2.3.1. Motor Units2.3.2. Factors that Influence the Force of Contraction2.3.2. Factors that Influence the Force of Muscle Contraction2.3.3. Energy Source for Muscle Contraction2.3.4. Skeletal Muscle Fiber Types2.3.5. Fatigue2.3.6. Muscle Pharmacology2.4. Smooth Muscle2.4.1. Smooth Muscle Contraction2.5. Control of Body Movement2.5.1. Voluntary Control of Muscle2.5.2. Reflexes2.6. Taste and Smell2.6.1. Taste2.6.2. The Sense of Smell2.7. Vision2.7.1. Structure of the Eye2.7.2. Focusing Light on the Retina2.7.3. Converting Light to Action Potentials2.7.4. The Retina2.7.5. Phototransduction2.7.6. Receptive Fields2.8. Hearing and Equilibrium2.8.1. The Nature of Sound2.8.2. The Hearing Apparatus2.8.3. Sound Vibrations to Action Potentials2.8.4. The Sense of Balance and EquilibriumModule 3.0. Cardiovascular System3.1. Structure of the Heart3.1.1. Chambers and Circulation3.2. Cardiac Cell Action Potentials3.2.1. Action Potentials in Cardiac Muscle Cells3.2.2. Action Potentials in Cardiac Autorhythmic cells3.2.3. Cellular Mechanisms of Inotropy and Chronotropy3.3. Electrophysiology of Heart Muscle3.3.1. Heart Conduction System3.3.2. Electrocardiogram (ECG)3.3.3. Abnormal ECG - Current of Injury3.4. The Cardiac Cycle3.4.1. Cardiac cycle3.4.2. Cardiac Measurements and Pressure Volume Loops3.5. Blood vessels and Blood Pressure3.5.1. Arteries and Veins3.5.2. Capillaries3.5.3. Blood Pressure Regulation and Shock3.5.4. Capillary Exchange3.5.5. Myogenic and Paracrine Regulation of Vasoconstriction and Vasodilation3.6. Blood3.6.1. Composition of Blood3.6.2. Hematopoeisis3.6.3. Breaking Down Red Blood Cells3.6.4. HemostasisModule 4.0. Urinary and Respiratory Systems4.1. Function and Structure of the Kidney4.1.1. Urinary System Function4.1.2. Functional Anatomy of the Urinary System4.1.3. The Nephron: Functional Unit of the Kidney4.1.4. The Renal Corpuscle: Bowman's Capsule4.2. Physiology of Urine Production4.2.1. Filtration4.2.2. Renal Clearance4.2.3. Tubular Reabsorption4.2.4. Urine Concentration and Dilution4.2.5. Hormonal Regulation of Urine Production4.3. Acid/Base Balance4.3.1. Buffers4.3.2. Acid/Base Disturbances4.4. The Respiratory System4.4.1. Respiratory System Structure and Function4.4.2. Respiratory Membrane4.4.3. Respiratory pressures and Inspriation/Expiration4.4.4. Alveoli and Surfactant4.4.5. Pneumothorax4.4.6. Pressure-Volume Loops and the Work of Breathing4.5. Gas Exchange and Transport4.5.1. Gas Laws4.5.2. Partial Pressure Gradients in the Lung4.5.3. Alveolar Gas Equation4.5.4. Oxygen and Carbon Dioxide Transport in the Blood4.5.5. Alveolar Ventilation4.5.6. Ventilation/Perfusion Ratio4.6. Chronic Bronchitis and Emphysema4.6.1. Respiratory Control by the Medulla Oblongata4.6.2. Chemicals that Regulate VentilationModule 5.0. Digestive, Endocrine and Reproductive Systems5.1. Functional Anatomy of the Digestive System5.1.1. Layers of the Digestive Tract5.1.2. Enteric Nervous System5.1.3. Organs of the Digestive System5.2. Digestion5.2.1. Carbohydrates5.2.2. Proteins5.2.3. Lipids5.2.4. Lipoproteins5.3. Regulation of Digestive Secretions5.4. Endocrine System5.4.1. Overview of the Endocrine System5.4.2. Hormone Receptors5.4.3. Hormones of the Body5.4.4. Other Hormones: Melatonin and Pheromones5.5. The Hypothalamus and Pituitary Gland5.5.1. Structure and Function of the Hypothalamus and Pituitary Gland5.5.2. The Posterior Pituitary5.5.3. The Anterior Pituitary5.5.4. Growth Hormone5.5.5. Prolactin5.5.6. Thyroid Hormones5.5.7. Adrenal Hormones5.6. Pancreas5.6.1. Insulin and Glucagon5.6.2. Diabetes Mellitus5.7. Reproductive System Anatomy5.7.1. Female Reproductive Anatomy5.7.2. Male Reproductive Anatomy5.7.3. Sexual Development at Puberty5.7.4. Male Reproductive Endocrine Axis5.7.5. Spermatogenesis5.7.6. Female Reproductive System: Oogenesis5.7.7. Ovulation and Fertilization5.7.8. The Ovarian Cycle5.7.9. The Uterine Cycle5.7.10. PregnancyAppendix A. GenderAppendix B. The Placebo EffectB.2.1. The Placebo EffectB.2.2. Examples of the Placebo EffectB.2.3. How do Placebos Work?B.2.4. Are Placebos Ethical?B.2.5. How do we validate actual effectiveness of placebosB.2.6. Tips for evaluating scientific evidenceB.2.7. What about Faith Healings
4.2.5

Hormonal Regulation of Urine Production

We have just discussed how the kidneys can generate gradients to reabsorb or secrete water, but the question still remains: how do the kidneys know when to reabsorb or secrete the water? This question will be answered in this section.

As previously mentioned, the principle cells of the collecting duct have aquaporin channels in the membranes of vesicles, essentially waiting for the signal for insertion into the plasma membrane. The hormone that induces insertion of the channels is called antidiuretic hormone (ADH; or arginine vasopressin). This hormone is produced by hypothalamic neurons and released from the posterior pituitary gland. There are three regulatory pathways to induce the release of ADH: Osmoreceptors, baroreceptors, and the renin-angiotensin-aldosterone system.

Osmoreceptors

The primary regulator of ADH secretion is blood osmolarity. Specialized nerve cells called osmoreceptors are located in the hypothalamus. These receptors are very sensitive to changes in blood ion concentrations. The area of the brain where they are located lacks the typical blood brain barrier and allows for easier access to ions. As a result, if the concentration of ions in the blood and interstitial fluids increases (conditions of dehydration), water moves out the osmoreceptors by osmosis to re-establish equilibrium. As the cells lose water they shrink and this shrinking induces action potentials. The action potentials are conducted to the posterior pituitary gland and stimulate the release of ADH.

Baroreceptors

Located within the walls of the aortic arch and carotid sinuses are specialized receptors called baroreceptors. These baroreceptors respond to stretch of the blood vessels which elicits action potentials in neurons to travel to the hypothalamus and synapse with hypothalamic neurons. Consequently, decreased blood pressure and lack of stretch of the baroreceptors in these vessels stimulate ADH secretion, while increased blood pressure (and subsequent increased strectch) decreases ADH secretion.

The Renin-Angiotensin-Aldosterone System

image164.png
Image by BYU-I Becky T F18
image165.png
Conversion of Angiotensin I to Angiotensin II increasing water reabsorption in kidney
https://cnx.org/resources/e20e7d6b1033f92c7ec59e78633956192c772da6/2626_Renin_Aldosterone_Angiotensin.jpg Author: OpenStax College License:  Creative Commons Attribution 3.0 Unported license.
image166.jpg
Image drawn by BYU-Idaho student Fall 2013
 
 image167.png
Renin-angiotensin-aldosterone system schematic.
 Author: By Soupvector (Own work) License: [CC BY-SA 4.0 (https://creativecommons.org/licenses/by-sa/4.0)], via Wikimedia Commons;  Link: https://commons.wikimedia.org/wiki/File%3ARenin-angiotensin-aldosterone_system.svg 

The three images above illustrate the renin-angiotensin-aldosterone system which promotes the direct retention of Na+, and thus, the indirect retention of water. The system starts with the release of renin, an enzyme produced by specialized cells of the afferent arteriole. Renin is released in response to a decrease in GFR (paracrine signaling) or a decrease in blood pressure (baroreceptors). In response to these stimuli, renin is released into the circulation. Renin is an enzyme that acts on a plasma protein called angiotensinogen. Angiotensinogen is produced by the liver and released into the circulation. As a result of the enzymatic cleavage by renin, angiotensin I is produced from angiotensinogen. Subsequently, angiotensin I is converted to angiotensin II by an enzyme called angiotensin-converting enzyme (ACE). Although ACE can be found in many tissues it is in especially high concentrations in the blood capillaries of the lungs. Angiotensin II has four major effects:

  1. It stimulates of the release of aldosterone from the adrenal gland (note: aldosterone release can also be directly stimulated by increased extracellular K+ levels)
  2. It preferentially constricts the efferent arteriole
  3. It is a potent vasoconstrictor of the systemic arterioles
  4. It induces the release of ADH from the posterior pituitary gland


These actions enhance Na+ reabsorption and water retention by the following mechanisms: Aldosterone is a hormone from the adrenal cortex that directly influences Na+/K+ ATPase by inducing the synthesis of new pumps and increasing the activity of existing pumps. Increasing the number and activity of this pump will greatly enhance the reabsorption of Na+ and the secretion of K+. Because of this effect on K+, aldosterone release is also tied to extracellular K+. If extracellular K+ levels increase, aldosterone is also released. If aldosterone levels are increased, the extracellular K+ concentrations will decrease. In some cases of excessive aldosterone the K+ levels can become dangerously low.

Constriction of the efferent arteriole will increase the pressure in the glomerular capillaries and thus increase the GFR. Increasing GFR will then promote increased filtration of Na+ thereby increasing the rate of reabsorption. Systemic vasoconstriction increases the mean arterial blood pressure. Because of the potent vasoconstricting effects of angiotensin II, a useful therapeutic tool to help reduce blood pressure is a family of drugs known as ACE inhibitors. By inhibiting the enzyme ACE, the production of angiotensin II is decreased, as its effect on blood pressure. Finally, inducing the release of ADH allows for the insertion of aquaporins and thus the increased reabsorption of water as it follows the increased sodium reabsorption. Based on these actions we can think of aldosterone as being primarily involved in regulating extracellular fluid volume due to its effects on Na+ reabsorption. Likewise, the primary role of ADH is regulating plasma osmolarity. These hormones can work in concert or they can function independently, depending on the needs of the body.

What if there is too much blood volume? Atrial natriuretic hormone (ANH) is a hormone produced by the atrial cells of the right atrium of the heart in response to stretch (high blood pressure).

In addition, brain natriuretic peptide (BNP) is produced by the ventricular cells of the heart and certain brain neurons, also in response to stretch. Once released these hormones act to decrease renin, aldosterone and vasopressin secretion. This results in an increase in both water and Na+ excretion by the kidney. These peptides also dilate the afferent arteriole enhancing the filtration rate.

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