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Carbohydrates and fats are the chief energy-giving foods. Proteins can give energy but are mainly used for building and repairing protoplasm. Weight More easily and quickly digested for weight, give twice as many energy and utilized than fats. Because it is the chief constitutent of protoplasm, tissues of plants and animals are the richest sources. These foods between them also contain other important body-building elements:e. Most of these substances cannot be manufactured in the body. They were thought to be 'amines essential to life'; hence named vitamines.

This name was changed to 'vitamin' when it was found that they were not all amines. Most vitamins function as coenzymes. Vitamin deficient diets can cause specific metabolic defects. Essentia I for regeneration of photopigments in retina. Cancer prevention. Is an antioxidant.

Yellow maize, peas, beans, carrots. In the liver, cholecalciferol is converted to 25hydroxycholecalciferol and, in the kidneys, this is hydroxylated to 1,25dihydroxycholecalciferol calcitriol. Found in liver of fish and animals, egg yolk and milk. Richest source - germ Involved in red blood of various cereals e. RNA formation. Helps adipose tissue and normal structure and muscle. Small amounts function of nervous in meat and dairy system and wound products. Calcitriol or 1,25 OHbD3 is the active from of vitamin D. Causes muscle dystrophy in monkeys and sterility in rats. May cause abnormalities of mitochondria, Iysosomes and plasma membrane.

Seeds and outer coats of grain e. Nuts e. Yeast and yeast extracts. Coenzyme for enzymes that break bonds between carbon atoms, Involved in metabolism of pyruvic acid to CO2 and H20 and in synthesis of acetylcholine.

Illustrated Physiology by B.R. Mackenna, Robin Callander, Ann B. McNaught (Paperback, 1996)

Decreased ATP formation in muscle and nerve, hence: 1. Component of coenzymes concerned with carbohydrate and protein metabolism in cells of eye, intestinal mucosa and blood. Most is excreted in urine, G. Cornea becomes cloudy. Cracks and fissures around lips and tongue. Component of coenzymes concerned with citric acid cycle, Inhibits production of cholesterol. Assists triglyceride breakdown,. Tongue red and sore in severe cases gastrointestinal upsets and mental derangement. Dermatitis of eyes, mouth, nose; nausea. Coenzyme for amino acid metabolism.

Helps produce circulating antibodies. Coenzyme in triglyceride metabolism. Produced by G,! Produced by G. Contains cobalt. Absorption from G. Rapidly destroyed by heat. Citrus fruits e. Tomatoes, rosehips, blackcurrants, red peppers, turnips and potatoes. Found in meat, liver. Secreted in milk. Impaired osteoblast activity,. Coenzyme involved in forming a constituent of collagen, Essential for formation and maintenance of intercellular cement and connective tissue, Especially necessary for healthy blood vessels, wound healing, bone growth, Functions as an antioxidant,?

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Cancer prevention,. Wounds heal slowly,. They differ only in detail. Amino group split Growth hormone sornarorrophin from the anterior pituitary enhances the entrance of amino acids into cell and stimulates building them intO protein. These actions favour growth. Lipids may be oxidised to produce ATP. Heart muscle oxidises fatty acid in preference to glucose for ATP. Tbe storage and oxidation of fat are endocrine. Growth hormone exerts its effect by the production of somatomedins by the liver. Organic molecules have chemical energy locked in their structure.

This energy can be transferred to adenosine triphosphate ATP when food molecules are broken down. From ATP the energy can be transferred to operate energy-requiring cell functions, e. Proteins, carbohydrates and fats can all provide energy for cells through ATP synthesis. In addition the products intermediates of each of these types of molecule can, to a large extent, provide the raw materials necessary to synthesize members of other classes.

NADH supplies electrons to the electron transport chain. This occurs when oxygen is available. The enzymes of the citric acid cycle are found inside mitochondria. Molecules of Acetyl coenzyme A enter the system and the 2-carbon acetyl fragment is passed on from enzyme to enzyme forming different compounds at each step. During aerobic respiration one molecule of glucose can generate molecules of ATP. The energy 'trapped' in ATP is used as required. Sodium, potassium etc. Many thousands of ATP molecules must release their energy to form one protein molecule.

Contraction of a muscle fibre requires expenditure of tremendous quantities of ATP. The body temperature is kept relatively constant with a slight fluctuation throughout the 24 hours in spite of wide variations in environmental temperature and heat production. Most of the energy released by oxidation of foodstuffs appears in the body as HEAT e. From lungs 2. Insensible Perspiration Diffusi 0 n th rou g h epidermis 2. Rectal temperature is about O. Unle-ss exercise is very strenuous or environment is very hot and humid these measures.

I ' by voluntary use 'Of t I I as.. Growth is most rapid before birth and during 1st year of life. A baby is born with epithelia, connective tissues, muscles, nerves and organs all present and formed - but all tissues do not grow at the same rate. Rapid growth of skeletal tissue during childhood. Nervous tissue develops rapidly in first 2 years. Most rapid growth is first at the head then legs begin to lengthen.

Thyroid hormone essential for brain development especially in first year. Inherited factors control pattern and limitations of growth. Nutrition: For optimal growth the body requires an adequate and balanced diet. Especially growth hormone, thyroid hormone, insulin, Endocrine glands: adrenal androgens, testicular testosterone, oestrogens.

Marked difference between sexes is initiated by gonadotrophin releasing hormone, luteinising hormone and follicle stimulating hormone of the anterior pituitary acting on sex glands and stimulating their production of oestrogen and testosterone. These hormones are largely responsible for development of secondary sex characteristics and development of reproductive organs. These hormones maintain secondary sex characteristics and reproductive ability during reproductive phase of adult life. BALANCED The individual's daily energy requirements are best obtained by eating well-balanced mews which contain carbohydrates, fat and protein plus vitamins, minerals and water.

Diet should contain about 70g protein, no more than 75g fat for men 53g for women and g carbohydrate per day. Choose lean, red meat. Remove fatty skin from chicken. White fish is low in fat: Oily fish contains essential fatty acids. Milk and dairy foods are important sources of calcium. Low fat varieties cut fat intake and still provide vitamins and minerals.

The more you eat the better. Contain vitamins A, C, E - the antioxidants which may protect against cancer. Also high in fibre and minerals. Gives fibre, vitamins, minerals: and essential fatty acids. I Polyunsatur: ated fats. Daily additional water requirement is about Litre. This vades with sweat loss, etc. See Index under 'Water Balance'. Transport through membranes takes several forms. Small uncharged molecules can diffuse between the phospholipid molecules of the membrane by random thermal motion.

This requires a concentration gradient. Ions can move down both a concentration and an electrical gradient, i.

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Because of their charge, ions cannot move between the phospholipid molecules. However some membrane proteins span the whole membrane and can form in their structure water-filled channels or pores which allow the passage of ions across the membrane, e. Movement through some channels is altered by the membrane potential see p. Other channels have receptors and are opened or closed by the binding of a hormone or neurotransmitter ligand-gated channels which alters the shape of the channel proteins.

Many channels remain open permanently. Other membrane proteins are called carrier proteins. The solute to be transported binds to the carrier which then changes its shape and by doing so moves the solute to the other side of the membrane. Glucose is an important substance transported by this mechanism. Little is known about the change in shape which takes place in the protein molecules. The diagram is not meant to indicate otherwise.

This is similar to the use of a waterfall to energize a water wheel to perform work. Solute binding site then becomes a low affinity tcone", site and solute dissociates. See page 4. Like the poles of a magnet, unlike charges are drawn towards each other. Like charges repel each other. If the numbers of positive and negative charges inside a cell were equal the inside of the cell would be electrically neutral. However, essentially all cells of the body have an excess of negative charges inside the cell and an excess of positive charges outside.

Inside is negative to the outside. The excess negative charge inside the cell and the excess positive charges outside the cell are attracted to each other. Hence the excess ions collect in a thin layer on the inside and outside surfaces of the plasma membrane. The bulk of the interstitial and intracellular fluid is electrically neutral. The potential difference across the membrane is measured in millivolts mV.

When the cell is not stimulated, the difference in potential is called the resting membrane potential. However, nerve and muscle cells are 'excitable', i. Nerves employ such potential changes to transmit signals along their membranes. In a nerve or muscle cell this will occur when the inside is about mV negative to the outside.

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The inside of the cell would then become more negative i. In the membrane there are separate channel proteins page 60 for each type of ion. These may be open or closed. The more channels that are open the greater will be the permeability of the membrane. The resting membrane potential of a nerve cell is about mV and of a skeletal muscle cell about mV. Most but not all cells are relatively permeable to Cl", They have Cl" channels but do not have cr pumps in their membrane. In such cells cr does not help to establish the resting membrane potential.

However the electrical force of the membrane potential moves Cl" to the positive outside of the membrane until a concentration gradient of Cl" builds up which has a diffusion force which equals the electrical force of the membrane potential and stops further net CI- movement. If the permeability of the membrane to CI- increases, since the Cl" concentration outside the cell is higher than inside, more cr will move into the cell making the cell more negative. If the inside of the cell becomes less negative i. If the inside of the cell becomes more negative the membrane is said to be hyperpolarized i.

Small localized changes in the potential of a membrane can occur with subthreshold stimuli. This change spreads only a few millimetres from the point of stimulation and quickly dies out. This is called electrotonic potential or the local response. When such a potential change occurs, current flows through the extracellular and intracellular fluids between the stimulated and unstimulated parts of the membrane. The direction of current flow is conventionally regarded as the direction in which positive ions move. Action potentials occur only when the membrane potential reaches a level at which depolarizing forces are greater than the repolarizing forces.

The membrane potential at which this occurs is called the threshold potential or the firing level. A stimulus which is just sufficiently large to produce this change is a threshold stimulus. This is followed by a rapid return to the resting membrane potential. In the resting membrane, most of the Na 1- channels are closed. Both these channel types are voltage-gated. As the membrane becomes less and less negative, more and more channels open.

The membrane potential is thus returned to its resting level. The action potential in nerve axons lasts about I ms millisecond. The threshold potential for most excitable cells is about 15 mV less negaflve than the resting membrane potential, In a nerve, if the membrane potential decreases from m V to m V the cell fires an action potential which propaga.

This triggers the next region of the membrane and the process is repeated again and again right along the nerve. The velocity of propagation depends on the diameter of the nerve fibre and whether or not the fibre is myelinated. The larger the fibre tbejaster is the propagation.

Consequently action potentials only occur where the myelin is interrupted, i. Thus the nerve impulse is propagated by leaping from node to node. This method of propagation is called saltatory conduction. Saltatory conduction causes a more rapid propagation in non-rnyelmated ax. ODS of the same diameter. Cells communicate with One another by sending messages in the form of chemicals to bring about a change in the.

Gap junctions A variety of cell types including cardiac muscle and smooth muscle have small channels linking their.. Small molecules and. Messages can be passed long distances via impulses in nerve axons. The nerve impulses liberate a neurotransm.

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Other nerves secrete neurohormones from their endings into the blood stream. The blood conveys the hormone 'to cells elsewhere In the body. Such a mechanism is used, e. Endocrine glands secrete hormones directly into the blood stream which then delivers the message to a large number of cells which are widely distributed. Chemical messengers may be released by cells and diffuse to neighbouring cells through the interstitial fluid, Such messengers are called paracrines.

Similarly other chemical messengers act on the cell that Autocrines secreted them. These are autocrines. Chemical messages activate the correct target cells because the target cells have specific protein molecules called receptors NB not sensory receptors, page to which the chemical messenger binds, Many receptors are located in the plasma membrane but some are on the nucleus and some are elsewhere in the cell.

The number of receptors in the membrane is not constant. Excess messenger often causes the number of receptors for that messenger to decrease. Tills is down regulation. A deficiency of chemical messenger can increase the number of receptors. This is up regulation. Such a change in activity may be e. All of these effects are brought about by an alteration in cell proteins e. The chemical messenger which binds to the receptor is called a first messenger or ligand.

The binding process activates the receptor which may then alter the permeability of a channel protein p. The effector protein may itself be an ion channel, tbe permeability of which is altered. More commonly the effector protein changes the concentration ofa mediator inside the cell which in turn alters the cell's activity. The intracellular mediator is called a second messenger.

One important second messenger is adenosine 3', S'-cyclic monophosphate cAMP which is formed from ATP by the action of the enzyme adenylate cyclase. Active cAMP-dependent Protein kinase A phosphorylates proteins which mediate the cell's response.


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A reduction of cAMP occurs when adenylate cyclase is inhibited by tbe binding of a ligand to an inhibitory receptor which in turn inhibits adenylate cyclase. When a ligand binds to a receptor which is coupled to a G protein, activation of the G protein occurs by guanosine triphosphate GTP displacing guanosine diphosphate GDP which is bound to the G protein when it is inactive.

G proteins are so-called because they strongly bind guanosine nucleotides p. AdenyJate cyclase is the most widely distributed effector protein and is responsible for converting ATP to the second messenger cAMP p.. A similar effector protein, 6 guanylate cyclase, generates guanosine 3', 5' cyclic monophosphate cGMP , another second messenger, which activates cGMP-dependent protein kinase protein kinase G. This second messenger system is not linked to so many receptors as the adenylate cyclasecAMP system. Secondly, a ligand may bind to a receptor which can activate, via a G protein, the membrane effector enzyme phospholipase C, which catalyses the formation of diacylglycerol DAG and inositol triphosphate IP3 from phospharidylinoaitol 4,5-diphosphate PIP2.

DAG activates protein kinase C which leads to altered cellular activity. Protein kinases are a class of enzymes that phosphorylate other proteins by transferring to them a phosphate group from ATP and, by so doing, alter their activity. This in tum alters the activity of the ceil. Marieb Science Research Awards at Mount Holyoke College, which promotes research by undergraduate science majors, and has underwritten renovation and updating of one of the biology labs in Clapp Laboratory at that college.

Marieb also contributes to the University of Massachusetts at Amherst where she generously provided funding for reconstruction and instrumentation of a cutting-edge cytology research laboratory. Recognizing the severe national shortage of nursing faculty, she underwrites the Nursing Scholars of the Future Grant Program at the university.

In , Dr. Marieb received the Benefactor Award from the National Council for Resource Development, American Association of Community Colleges, which recognizes her ongoing sponsorship of student scholarships, faculty teaching awards, and other academic contributions to Holyoke Community College. In May , the science building at Holyoke Community College was named in her honor. Additionally, while actively engaged as an author, Dr. When not involved in academic pursuits, Dr.

Marieb is a world traveler and has vowed to visit every country on this planet. She is an enthusiastic supporter of the local arts and enjoys a competitive match of doubles tennis. Her teaching excellence has been recognized by several awards during her 21 years at Mount Royal University. Hoehn received her M. Prize for excellence in medical research. During her Ph. Hoehn has been a contributor to several books and has written numerous research papers in Neuroscience and Pharmacology. Following Dr. Hoehn provides financial support for students in the form of a scholarship that she established in for nursing students at Mount Royal University.

When not teaching, she likes to spend time outdoors with her husband and two sons, compete in triathlons, and play Irish flute. Cloth Bound with Access Card. We're sorry! We don't recognize your username or password. Please try again. The work is protected by local and international copyright laws and is provided solely for the use of instructors in teaching their courses and assessing student learning. You have successfully signed out and will be required to sign back in should you need to download more resources.

Elaine N. Preface Preface is available for download in PDF format. Why This Matters Video Activities feature clinicians talking about how the content of each chapter applies to what they do in the field every day. Full-color animations demonstrate difficult concepts, and engaging activities help reinforce the material. Seamlessly integrated videos and other rich media. Accessible screen-reader ready. Configurable reading settings, including resizable type and night reading mode. Instructor and student note-taking, highlighting, bookmarking, and search. Dynamic Study Modules help students study effectively on their own by continuously assessing their activity and performance in real time.

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Consequently, prolonged vomiting may lead to hypokalemia. At all rates of secretion, Cl - is the major anion of gastric juice. At high rates of secretion, gastric juice resembles an isotonic solution of HCl. Gastric HCl converts pepsinogens to active pepsins and provides the acid pH at which pepsins are active. The basal rate is greater at night and lowest in the early morning. The total number of parietal cells in the stomach of normal individuals varies greatly, and this variation is partly responsible for the wide range in basal and stimulated rates of HCl secretion.

Organic Constituents of Gastric Juice. Table The predominant organic constituent of gastric juice is pepsinogen, the inactive proenzyme of pepsin. Pepsins, often collectively called "pepsin," are a group of proteases secreted by the chief cells of the gastric glands. Pepsinogens are contained in membrane-bound zymogen granules in the chief cells. Zymogen granules release their contents by exocytosis when chief cells are stimulated to secrete Table Pepsinogens are converted to active pepsins by the cleavage of acid-labile linkages. The lower the pH, the more rapid the conversion.

Pepsins also act proteolytically on pepsinogens to form more pepsin. Pepsins are most proteolytically active at pH 3 and below. When the pH of the duodenal lumen is neutralized, pepsins are inactivated by the neutral pH. Intrinsic factor, a glycoprotein secreted by parietal cells of the stomach, is required for the normal absorption of vitamin B Intrinsic factor is released in response to the same stimuli that elicit the secretion of HCl by parietal cells. Secretion of intrinsic factor is the only gastric function that is essential for human life. Cellular Mechanisms of Gastric Acid Secretion.

Parietal cells have a distinctive ultrastructure Fig. Branching secretory canaliculi course through the cytoplasm and are connected by a common outlet to the cell's luminal surface. Microvilli line the surfaces of the secretory canaliculi. The cytoplasm of unstimulated parietal cells contains numerous tubules and vesicles, which is called the tubulovesicular system. When parietal cells are stimulated to secrete HCl Fig. Thus, the pH is 7 in the parietal cell cytosol and 1 in the lumen of the gastric gland. Figure Parietal cell ultrastructure. A, A resting parietal cell showing the tubulovesicular apparatus in the cytoplasm and the intracellular canaliculus.

B, An activated parietal cell that is secreting acid. The tubulovesicles have fused with the membranes of the intracellular canaliculus, which is now open to the lumen of the gland and lined with abundant long microvilli. Cl - enters the lumen via an ion channel a ClC Cl - channel located in the luminal membrane.

Secretion of HCO 3 -. HCO 3 - is entrapped by the viscous mucus that coats the surface of the stomach; thus, the mucus secreted by the resting mucosa lines the stomach with a sticky, alkaline coat. When food is eaten, moreover, rates of secretion of both mucus and HCO 3 - increase. Secretions that contain mucins are viscous and sticky and are collectively termed mucus. Mucins are secreted by mucous neck cells located in the necks of gastric glands and by the surface epithelial cells of the stomach. Mucus is stored in large granules in the apical cytoplasm of mucous neck cells and surface epithelial cells and is released by exocytosis.

Figure Schematic representation of the structure of gastric mucins before and after hydrolysis by pepsin. Intact mucins are tetramers of four similar monomers of about , Da. Each monomer is largely covered by carbohydrate side chains that protect it from proteolytic degradation. The central portion of the mucin tetramer, near the disulfide cross-links, is more susceptible to proteolytic digestion. Pepsins cleave bonds near the center of the tetramers to release fragments about the size of monomers.

These tetrameric mucins form a sticky gel that adheres to the surface of the stomach. However, this gel is subject to proteolysis by pepsins, which cleave disulfide bonds near the center of the tetramers. Proteolysis releases fragments that do not form gels and thus dissolves the protective mucus layer.

Maintenance of the protective mucus layer requires continuous synthesis of new tetrameric mucins to replace the mucins that are cleaved by pepsins.


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Mucus is secreted at a significant rate in the resting stomach. Secretion of mucus is stimulated by some of the same stimuli that enhance acid and pepsinogen secretion, especially acetylcholine released from parasympathetic nerve endings near the gastric glands. If the gastric mucosa is mechanically deformed, neural reflexes are evoked to enhance mucus secretion.

Extrinsic efferent fibers terminate on intrinsic neurons that innervate parietal cells, ECL cells that secrete the paracrine mediator histamine, and endocrine cells that secrete the hormone gastrin. In addition, vagal stimulation results in the secretion of pepsinogen, mucus, HCO 3 - , and intrinsic factor.

Stimulation of the parasympathetic nervous system also occurs during the cephalic and oral phase of the meal. However, the gastric phase produces the largest stimulation of gastric secretion of the postprandial period Fig. Stimulation of gastric acid secretion is an excellent example of a "feed forward" or cascade response that uses endocrine, paracrine, and neural pathways.

Activation of intrinsic neurons by vagal efferent activity results in the release of acetylcholine from nerve terminals, which activates cells in the gastric epithelium. In addition, parasympathetic activation, via gastrin-releasing peptide from intrinsic neurons, releases gastrin from G cells located in the gastric glands in the gastric antrum Fig.

Parietal cells express cholecystokinin type 2 CCK2 receptors for gastrin. Histamine is also secreted in response to vagal nerve stimulation, and ECL cells express muscarinic and gastrin receptors. Thus, gastrin and vagal efferent activity induce the release of histamine, which potentiates the effects of both gastrin and acetylcholine on the parietal cell. Hence, activation of parasympathetic vagal outflow to the stomach is very efficient at stimulating the parietal cell to secrete acid Fig. In the gastric phase, the presence of food in the stomach is detected and activates vagovagal reflexes to stimulate secretion.

Food in the stomach results in distention and stretch, which are detected by afferent or sensory nerve endings in the gastric wall. These are the peripheral terminals of vagal afferent nerves that transmit information to the brainstem and thereby drive activity in vagal efferent fibers, a vagovagal reflex Fig. In addition, digestion of proteins increases the concentration of oligopeptides and free amino acids in the lumen, which are detected by chemosensors in the gastric mucosa. Oligopeptides and amino acids also stimulate vagal afferent activity.

The exact nature of the chemosensors is not clear but may involve endocrine cells that release their contents to activate nerve endings. This topic will be discussed in more detail in Chapter Figure Neural regulation of gastric acid secretion in the gastric phase of the meal is mediated by the vagus nerve. The stimulation that occurs in the cephalic and oral phases, before food reaches the stomach, results in stimulation of parietal cells to secrete acid and chief cells to secrete pepsinogen. Thus, when food reaches the stomach, protein digestion is initiated by generating protein hydrolysate, which further stimulates the secretion of gastrin from the mucosa of the gastric antrum.

In addition, gastric distention activates a vagovagal reflex that further stimulates gastric acid and pepsinogen secretion. Figure The parietal cell is regulated by neural, hormonal, and paracrine pathways. Activation of vagal parasympathetic preganglionic outflow to the stomach acts in three ways to stimulate gastric acid secretion. There is direct neural innervation and activation of the parietal cell via release of acetylcholine ACh from enteric neurons, which acts on the parietal cell via muscarinic receptors.

In addition, neural activation of the ECL cell stimulates the release of histamine, which acts via a paracrine pathway to stimulate the parietal cell. Finally, G cells located in gastric glands in the gastric antrum are activated by the release of gastrin-releasing peptide from enteric neurons, which acts on the G cell to stimulate the release of gastrin. Gastrin thereafter acts via a humoral pathway to stimulate the parietal cell.

Somatostatin has a paracrine action on neighboring G cells to decrease the release of gastrin and thereby decrease gastric acid secretion Fig. Figure Feedback regulation of gastric acid secretion by release of somatostatin and its action on G cells in the gastric antrum. This in turn acts on specific receptors on G cells to inhibit the release of gastrin and thus bring about inhibition of gastric acid secretion.

Figure Vagal parasympathetic stimulation of gastric secretions via enteric neurons. Vagal preganglionic neurons innervate the myenteric and submucosal plexus; the terminals of the vagal preganglionic neurons innervate many enteric neurons and thus bring about changes in function as described in Figure Figure Signal transduction mechanisms showing the mechanism of action of agonists secretagogues and antagonists that regulate secretion in parietal cells.

Acetylcholine ACh binds to muscarinic M 3 receptors. Histamine acts via the H 2 receptor. Gastrin binds to the cholecystokinin type 2 CCK2 receptor. Activation of H 2 receptors activates adenylyl cyclase to increase intracellular levels of cAMP.