The Posterior Lobe

The posterior lobe of the pituitary releases two hormones, both synthesized in the hypothalamus, into the circulation.

• Antidiuretic Hormone (ADH).
  ADH is a peptide of 9 amino acids. It is also known as arginine vasopressin. ADH acts on the collecting ducts of the kidney to facilitate the reabsorption of water into the blood.
  • A deficiency of ADH
    • leads to excessive loss of urine, a condition known as diabetes  nsipidus.
• Oxytocin
  Oxytocin is a peptide of 9 amino acids. Its principal actions are:
  • stimulating contractions of the uterus at the time of birth
  • stimulating release of milk when the baby begins to suckle

Basic Properties of Gases

A.    Dalton's Law of Partial Pressures

1.    partial pressure - the "part" of the total air pressure caused by one component of a gas 

     Gas            Percent            Partial Pressure (P)
    ALL AIR        100.0%                760 mm Hg
    Nitrogen       78.6%                   597 mm Hg    (0.79 X 760)
    Oxygen          20.9%                l59 mm Hg    (0.21 X 760)
    CO₂              0.04%                  0.3 mm Hg    (0.0004 X 760) 

2.    altitude - air pressure @ 10,000 ft = 563 mm Hg
3.    scuba diving - air pressure @ 100 ft = 3000 mm Hg

B.    Henry's Law of Gas Diffusion into Liquid

1.    Henry's Law - a certain gas will diffuse INTO or OUT OF a liquid down its concentration gradient in proportion to its partial pressure

2.    solubility - the ease with which a certain gas will "dissolve" into a liquid (like blood plasma)

HIGHest solubility in plasma            Carbon Dioxide
                                                      Oxygen
                                        
LOWest solubility in plasma             Nitrogen

C.    Hyperbaric (Above normal pressure) Conditions

1.    Creates HIGH gradient for gas entry into the body

2.    therapeutic - oxygen forced into blood during: carbon monoxide poisoning, circulatory shock, asphyxiation, gangrene, tetanus, etc.

3.    harmful - SCUBA divers may suffer the "bends" when they rise too quickly and Nitrogen gas "comes out of solution" and forms bubbles in the blood

The Nerve Impulse

When a nerve is stimulated the resting potential changes. Examples of such stimuli are pressure, electricity, chemicals, etc. Different neurons are sensitive to different stimuli(although most can register pain). The stimulus causes sodium ion channels to open. The rapid change in polarity that moves along the nerve fiber is called the "action potential." In order for an action potential to occur, it must reach threshold. If threshold does not occur, then no action potential can occur. This moving change in polarity has several stages:

Depolarization

The upswing is caused when positively charged sodium ions (Na+) suddenly rush through open sodium gates into a nerve cell. The membrane potential of the stimulated cell undergoes a localized change from -55 millivolts to 0 in a limited area. As additional sodium rushes in, the membrane potential actually reverses its polarity so that the outside of the membrane is negative relative to the inside. During this change of polarity the membrane actually develops a positive value for a moment(+30 millivolts). The change in voltage stimulates the opening of additional sodium channels (called a voltage-gated ion channel). This is an example of a positive feedback loop.

Repolarization

The downswing is caused by the closing of sodium ion channels and the opening of potassium ion channels. Release of positively charged potassium ions (K+) from the nerve cell when potassium gates open. Again, these are opened in response to the positive voltage--they are voltage gated. This expulsion acts to restore the localized negative membrane potential of the cell (about -65 or -70 mV is typical for nerves).

Hyperpolarization

When the potassium ions are below resting potential (-90 mV). Since the cell is hyper polarized, it goes to a refractory phrase.

Refractory phase

The refractory period is a short period of time after the depolarization stage. Shortly after the sodium gates open, they close and go into an inactive conformation. The sodium gates cannot be opened again until the membrane is repolarized to its normal resting potential. The sodium-potassium pump returns sodium ions to the outside and potassium ions to the inside. During the refractory phase this particular area of the nerve cell membrane cannot be depolarized. This refractory area explains why action potentials can only move forward from the point of stimulation.

Factors that affect sensitivity and speed

Sensitivity

Increased permeability of the sodium channel occurs when there is a deficit of calcium ions. When there is a deficit of calcium ions (Ca+2) in the interstitial fluid, the sodium channels are activated (opened) by very little increase of the membrane potential above the normal resting level. The nerve fiber can therefore fire off action potentials spontaneously, resulting in tetany. This could be caused by the lack of hormone from parathyroid glands. It could also be caused by hyperventilation, which leads to a higher pH, which causes calcium to bind and become unavailable.

Speed of Conduction

This area of depolarization/repolarization/recovery moves along a nerve fiber like a very fast wave. In myelinated fibers, conduction is hundreds of times faster because the action potential only occurs at the nodes of Ranvier (pictured below in 'types of neurons') by jumping from node to node. This is called "saltatory" conduction. Damage to the myelin sheath by the disease can cause severe impairment of nerve cell function. Some poisons and drugs interfere with nerve impulses by blocking sodium channels in nerves. See discussion on drug at the end of this outline.

Regulation of Blood Pressure by Hormones

The Kidney

One of the functions of the kidney is to monitor blood pressure and take corrective action if it should drop. The kidney does this by secreting the proteolytic enzyme renin.

• Renin acts on angiotensinogen, a plasma peptide, splitting off a fragment containing 10 amino acids called angiotensin I.
• angiotensin I is cleaved by a peptidase secreted by blood vessels called angiotensin converting enzyme (ACE) — producing  angiotensin II, which contains 8 amino acids.
• angiotensin II
  • constricts the walls of arterioles closing down capillary beds;
  • stimulates the proximal tubules in the kidney to reabsorb sodium ions;
  • stimulates the adrenal cortex to release aldosterone. Aldosterone causes the kidneys to reclaim still more sodium and thus water.
  • increases the strength of the heartbeat;
  • stimulates the pituitary to release the antidiuretic hormone (ADH, also known as arginine vasopressin).

All of these actions, which are mediated by its binding to G-protein-coupled receptors on the target cells, lead to an increase in blood pressure.

Contractility : Means ability of cardiac muscle to convert electrical energy of action potential into mechanical energy ( work).
The excitation- contraction coupling of cardiac muscle is similar to that of skeletal muscle , except the lack of motor nerve stimulation. 

Cardiac muscle is a self-excited muscle , but the principles of contraction are the same . There are many rules that control the contractility of the cardiac muscles, which are:

1. All or none rule: due to the syncytial nature of the cardiac muscle.There are atrial syncytium and ventricular syncytium . This rule makes the heart an efficient pump.

2. Staircase phenomenon : means gradual increase in muscle contraction following rapidly repeated stimulation..

3. Starling`s law of the heart: The greater the initial length of cardiac muscle fiber , the greater the force of contraction. The initial length is determined by the degree of diastolic filling .The pericardium prevents overstretching of heart , and allows optimal increase in diastolic volume.

Thankful to this law , the heart is able to pump any amount of blood that it receives. But overstretching of cardiac muscle fibers may cause heart failure.

Factors affecting  contractility ( inotropism)

I. Positive inotropic factors:

1. sympathetic stimulation: by increasing the permeability of sarcolemma to calcium.
2. moderate increase in temperature . This due to increase metabolism to increase ATP , decrease viscosity of myocardial structures, and increasing calcium influx.
3. Catecholamines , thyroid hormone, and glucagon hormones.
4. mild alkalosis
5. digitalis
6. Xanthines ( caffeine and theophylline )

II. Negative inotropic factors:

1. Parasympathetic stimulation : ( limited to atrial contraction)
2. Acidosis
3. Severe alkalosis
4. excessive warming and cooling .
5. Drugs ;like : Quinidine , Procainamide , and barbiturates .
6. Diphtheria and typhoid toxins.

Vital Capacity: The vital capacity (VC) is the maximum volume which can be ventilated in a single breath. VC= IRV+TV+ERV. VC varies with gender, age, and body build. Measuring VC gives a device for diagnosis of respiratory disorder, and a benchmark for judging the effectiveness of treatment. (4600 ml)

Vital Capacity is reduced in restrictive disorders, but not in disorders which are purely obstructive.

The FEV₁ is the % of the vital capacity which is expelled in the first second. It should be at least 75%. The FEV₁ is reduced in obstructive disorders.

Both VC and the FEV₁ are reduced in disorders which are both restrictive and obstructive

Oxygen is present at nearly 21% of ambient air. Multiplying .21 times 760 mmHg (standard pressure at sea level) yields a pO₂ of about 160. Carbon dioxide is .04% of air and its partial pressure, pCO₂, is .3.

With alveolar air having a pO₂ of 104 and a pCO₂ of 40. So oxygen diffuses into the alveoli from inspired air and carbon dioxide diffuses from the alveoli into air which will be expired. This causes the levels of oxygen and carbon dioxide to be intermediate in expired air when compared to inspired air and alveolar air. Some oxygen has been lost to the alveolus, lowering its level to 120, carbon dioxide has been gained from the alveolus raising its level to 27.

Likewise a concentration gradient causes oxygen to diffuse into the blood from the alveoli and carbon dioxide to leave the blood. This produces the levels seen in oxygenated blood in the body. When this blood reaches the systemic tissues the reverse process occurs restoring levels seen in deoxygenated blood.