Events in gastric function:

1) Signals from vagus nerve begin gastric secretion in cephalic phase.

2) Physical contact by food triggers release of pepsinogen and H⁺ in gastric phase.

3) Muscle contraction churns and liquefies chyme and builds pressure toward pyloric sphincter.

4) Gastrin is released into the blood by cells in the pylorus. Gastrin reinforces the other stimuli and acts as a positive feedback mechanism for secretion and motility.

5) The intestinal phase begins when acid chyme enters the duodenum. First more gastrin secretion causes more acid secretion and motility in the stomach.

6) Low pH inhibits gastrin secretion and causes the release of enterogastrones such as GIP into the blood, and causes the enterogastric reflex. These events stop stomach emptying and allow time for digestion in the duodenum before gastrin release again stimulates the stomach.

Production of Hormones

The kidneys produce and interact with several hormones that are involved in the control of systems outside of the urinary system.

Calcitriol. Calcitriol is the active form of vitamin D in the human body. It is produced by the kidneys from precursor molecules produced by UV radiation striking the skin. Calcitriol works together with parathyroid hormone (PTH) to raise the level of calcium ions in the bloodstream. When the level of calcium ions in the blood drops below a threshold level, the parathyroid glands release PTH, which in turn stimulates the kidneys to release calcitriol. Calcitriol promotes the small intestine to absorb calcium from food and deposit it into the bloodstream. It also stimulates the osteoclasts of the skeletal system to break down bone matrix to release calcium ions into the blood.
 
Erythropoietin. Erythropoietin, also known as EPO, is a hormone that is produced by the kidneys to stimulate the production of red blood cells. The kidneys monitor the condition of the blood that passes through their capillaries, including the oxygen-carrying capacity of the blood. When the blood becomes hypoxic, meaning that it is carrying deficient levels of oxygen, cells lining the capillaries begin producing EPO and release it into the bloodstream. EPO travels through the blood to the red bone marrow, where it stimulates hematopoietic cells to increase their rate of red blood cell production. Red blood cells contain hemoglobin, which greatly increases the blood’s oxygen-carrying capacity and effectively ends the hypoxic conditions.
 
Renin. Renin is not a hormone itself, but an enzyme that the kidneys produce to start the renin-angiotensin system (RAS). The RAS increases blood volume and blood pressure in response to low blood pressure, blood loss, or dehydration. Renin is released into the blood where it catalyzes angiotensinogen from the liver into angiotensin I. Angiotensin I is further catalyzed by another enzyme into Angiotensin II.

Angiotensin II stimulates several processes, including stimulating the adrenal cortex to produce the hormone aldosterone. Aldosterone then changes the function of the kidneys to increase the reabsorption of water and sodium ions into the blood, increasing blood volume and raising blood pressure. Negative feedback from increased blood pressure finally turns off the RAS to maintain healthy blood pressure levels.

Neurophysiology

Transmission of an action potential. This occurs in two ways:

1) across the synapse - synaptic transmission. This is a chemical process, the result of a chemical neurotransmitter.

2) along the axon - membrane transmission. This is the propagation of the action potential itself along the membrane of the axon.

Synaptic transmission - What you learned about the neuromuscular junction is mostly applicable here as well. The major differences in our current discussion are:

1) Transmission across the synapse does not necessarily result in an action potential. Instead, small local potentials are produced which must add together in summation to produce an action potential.

2) Although ACh is a common neurotransmitter, there are many others and the exact effect at the synapse depends on the neurotransmitter involved.

3) Neurotransmitters can be excitatory or inhibitory. The result might be to turn off the next neuron rather than to produce an action potential

The basic steps of synaptic transmission are the same as described at the neuromuscular junction

1) Impulse arrives at the axon terminus causing opening of Ca²⁺ channels and allows Ca²⁺  to enter the axon. The calcium ions are in the extracellular fluid, pumped there much like sodium is pumped. Calcium is just an intermediate in both neuromuscular and synaptic transmission.

2) Ca²⁺  causes vesicles containing neurotransmitter to release the chemical into the synapse by exocytosis across the pre-synaptic membrane.

3) The neurotransmitter binds to the post-synaptic receptors. These receptors are linked to chemically gated ion channels and these channels may open or close as a result of binding to the receptors to cause a graded potential which can be either depolarization, or hyperpolarization depending on the transmitter. Depolarization results from opening of Na⁺ gates and is called an EPSP. Hyperpolarization could result from opening of K⁺ gates and is called IPSP. 

4) Graded potentials spread and overlap and can summate to produce a threshold depolarization and an action potential when they stimulate voltage gated ion channels in the neuron's trigger region.

5) The neurotransmitter is broken down or removed from the synapse in order for the receptors to receive the next stimulus. As we learned there are enzymes for some neurotransmitters such as the Ach-E which breaks down acetylcholine. Monoamine oxidase (MAO) is an enzyme which breaks down the catecholamines (epinephrine, nor-epinephrine, dopamine) and nor-epinephrine (which is an important autonomic neurotransmitter) is removed by the axon as well in a process known as reuptake. Other transmitters may just diffuse away.

Graded Potentials - these are small, local depolarizations or hyperpolarizations which can spread and summate to produce a threshold depolarization. Small because they are less than that needed for threshold in the case of the depolarizing variety. Local means they only spread a few mm on the membrane and decline in intensity with increased distance from the point of the stimulus. The depolarizations are called EPSPs, excitatory post-synaptic potentials, because they tend to lead to an action potential which excites or turns the post-synaptic neuron on. Hyperpolarizations are called IPSPs, inhibitory post-synaptic potentials, because they tend to inhibit an action potential and thus turn the neuron off.

Summation - the EPSPs and IPSPs will add together to produce a net depolarization (or hyperpolarization).

Temporal summation- this is analogous to the frequency (wave, tetany) summation discussed for muscle. Many EPSPs occurring in a short period of time (e.g. with high frequency) can summate to produce threshold depolarization. This occurs when high intensity stimulus results in a high frequency of EPSPs.

Spatial summation - this is analogous to quantal summation in a muscle. It means that there are many stimuli occurring simultaneously. Their depolarizations spread and overlap and can build on one another to sum and produce threshold depolarization.

Inhibition - When the brain causes an IPSP in advance of a reflex pathway being stimulated, it reduces the likelihood of the reflex occurring by increasing the depolarization required. The pathway can still work, but only with more than the usual number or degree of stimulation. We inhibit reflexes when allowing ourselves to be given an injection or blood test for instance.

Facilitation - When the brain causes an EPSP in advance of a reflex pathway being stimulated, it makes the reflex more likely to occur, requiring less additional stimulation. When we anticipate a stimulus we often facilitate the reflex.

Learned Reflexes - Many athletic and other routine activities involve learned reflexes. These are reflex pathways facilitated by the brain. We learn the pathways by performing them over and over again and they become facilitated. This is how we can perfect our athletic performance, but only if we learn and practice them correctly. It is difficult to "unlearn" improper techniques once they are established reflexes. Like "riding a bike" they may stay with you for your entire life!

Post-tetanic potentiation - This occurs when we perform a rote task or other repetitive action. At first we may be clumsy at it, but after continuous use (post-tetanic) we become more efficient at it (potentiation). These actions may eventually become learned reflexes

The Action Potential

The trigger region of a neuron is the region where the voltage gated channels begin. When summation results in threshold depolarization in the trigger region of a neuron, an action potential is produced. There are both sodium and potassium channels. Each sodium channel has an activation gate and an inactivation gate, while potassium channels have only one gate. 

A) At the resting state the sodium activation gates are closed, sodium inactivation gates are open, and potassium gates are closed. Resting membrane potential is at around -70 mv inside the cell. 

B) Depolarizing phase: The action potential begins with the activation gates of the sodium channels opening, allowing Na+ ions to enter the cell and causing a sudden depolarization which leads to the spike of the action potential. Excess Na+ ions enter the cell causing reversal of potential becoming briefly more positive on the inside of the cell membrane.

C) Repolarizing phase: The sodium inactivation gates close and potassium gates open. This causes Na+ ions to stop entering the cell and  K+ ions  to leave the cell, causing repolarization. Until the membrane is repolarized it cannot be stimulated, called the absolute refractory period.

D) Excess potassium leaves the cell causing a brief hyperpolarization. Sodium activation gates close and potassium gates begin closing. The sodium-potassium pump begins to re-establish the resting membrane potential. During hyperpolarization the membrane can be stimulated but only with a greater than normal depolarization, the relative refractory period.

Action potentials are self-propagated, and once started the action potential progresses along the axon membrane. It is all-or-none, that is there are not different degrees of action potentials. You either have one or you don't.

Carbohydrates:

• about 3% of the dry mass of a typical cell
• composed of carbon, hydrogen, & oxygen atoms (e.g., glucose is C₆H₁₂O₆)
• an important source of energy for cells
• types include:
  • monosaccharide (e.g., glucose) - most contain 5 or 6 carbon atoms
  • disaccharides
    • 2 monosaccharides linked together
    • Examples include sucrose (a common plant disaccharide is composed of the monosaccharides glucose and fructose) & lactose (or milk sugar; a disaccharide composed of glucose and the monosaccharide galactose)
  • polysaccharides
    • several monosaccharides linked together

Examples include starch (a common plant polysaccharide made up of many glucose molecules) and glycogen (commonly stored in the liver)

Typical Concentration Gradients and Membrane Potentials in Excitable Cells

The Na Pump is Particularly Important in the Kidney and Brain

• All cells have Na pumps in their membranes, but some cells have more than others
• Over-all Na pump activity may account for a third of your resting energy expenditure!
• In the kidney the Na pump activity is very high because it is used to regulate body salt and water concentrations
  • Kidneys use enormous amounts of energy: 0.5% of body weight, but use 7% of the oxygen supply
• Pump activity is also high in the brain because Na and K gradients are essential for nerves
  • The brain is another high energy organ; it is 2% of body weight, but uses 18% of the oxygen supply

In the Resting State Potassium Controls the Membrane Potential of Most Cells

• Resting cells have more open K channels than other types
• More K+ passes through membrane than other ions- therefore K+ controls the potential
• Blood K+ must be closely controlled because small changes will produce large changes in the membrane potentials of cells
  • Raising K will make the membrane potential less negative (depolarization)
• High blood K+ can cause the heart to stop beating (it goes into permanent contraction)

During an Action Potential Na Channels Open, and Na Controls the Membrane Potential

• Whichever ion has the most open channels controls the membrane potential
• Excitable cells have Na channels that open when stimulated
• When large numbers of these channels open Na controls the membrane potential

Ventilation simply means inhaling and exhaling of air from the atmospheric air into lungs and then exhaling it from the lung into the atmospheric air.
Air pressure gradient has to exist between two atmospheres to enable a gas to move from one atmosphere to an other.
 

During inspiration: the intrathoracic pressure has to be less than that of atmospheric pressure. This could be achieved by decreasing the intrathoracic pressure as follows:
 

Depending on Boyle`s law , the pressure of gas is inversely proportional to the volume of its container. So increasing the intrathoracic volume will decrease the intrathoracic pressure which will allow the atmospheric air to be inhaled (inspiration) . As decreasing the intrathoracic volume will increase the intrathoracic pressure and causes exhaling of air ( expiration)

So. Inspiration  could be actively achieved by the contraction of inspiratory muscles : diaphragm and intercostal muscles. While relaxation of the mentioned muscles will passively cause expiration.
 

Contraction of diaphragm will pull the diaphragm down the abdominal cavity ( will move inferiorly)  , and then increase the intrathoracic volume ( vertically)  . Contraction of external intercostal muscle will pull the ribs upward and forward which will additionally increase the intrathoracic volume ( transversely  , the net result will be increasing the intrathoracic volume and decreasing the intrathoracic pressure.
 

Relaxation of diaphragm will move it superiorly during expiration, the relaxation of external intercostal muscles will pull the ribs downward and backward , and the elastic lungs and chest wall will recoil. The net result is decreasing the intrathoracic volume and increasing intrathoracic pressure.
 

All of this occurs during quiet breathing. During forceful inspiration an accessory inspiratory muscle will be involved ( scaleni , sternocleidomastoid , and others) to increase negativity in the intrathoracic pressure more and more.
 

During forceful expiration the accessory expiratory muscles ( internal intercostal muscles and abdominal muscles ) will be involved to decrease the intrathoracic volume  more and more and then to increase  intrathoracic pressure more and more.

The pressure within the alveoli is called intralveolar  pressure . Between the two phases of respiration it is equal to the atmospheric pressure. It is decreased during inspiration ( about 1 cm H₂O ) and increased during expiration ( about +1 cm H₂O ) . This difference allow entering of 0.5 L of air into the lungs.

Intrapleural pressure is the pressure of thin fluid between the two pleural layers . It is a slight negative pressure. At the beginning of inspiration it is about -5 cm H2O and reachs -7.5 cm H₂O at the end or inspiration.

At the beginning of expiration the intrapleural pressure is -7.5 cm H₂O and reaches -5 cmH₂O at the end of expiration.
The difference between intralveolar pressure and intrapleural pressure is called transpulmonary pressure.

Factors , affecting ventilation :
 

Resistance : Gradual decreasing of the diameter of respiratory airway increase the resistance to air flow.
 

Compliance : means the ease , which the lungs expand.It depends on both the elastic forces of the lungs and the elastic forces , caused by the the surface tension of the fluid, lining the alveoli.
 

Surface tension: Molecules of water have tendency to attract each other on the surface of water adjacent to air. In alveoli the surface tension caused by the fluid in the inner surface of the alveoli  may cause collapse of alveoli . The surface tension is decreased by the surfactant .

Surfactant is a mixture of phospholipids , proteins and ion m produced by type II pneumocytes.

Immature newborns may suffer from respiratory distress syndrome , due to lack of surfactant which is produced during the last trimester of pregnancy.
 

The elastic fibers of the thoracic wall also participate in lung compliance.