RECEPTORS ACT AS ON/OFF BUTTONS THAT CONTROL THE VARIOUS SYMPATHETIC AND PARASYMPATHETIC EFFECTS IN THE BODY.

A] SYMPATHETIC OR ADRENERGIC RECEPTOR –

1] Alpha-receptors are located on the arteries. When the alpha receptor is stimulated, the arteries constrict.

2] Beta 1 receptors are located in the heart. When Beta 1 receptors are stimulated, they increase the heart rate and increase the heart's strength of contraction or contractility.

3] Beta 2 receptors are located in the bronchioles of the lungs and the arteries of the skeletal muscles. When these receptors are stimulated, they increase the diameter of the bronchioles to let more air in
and out during breathing and they dilate the vessels of the skeletal muscles so they can receive the increased blood flow produced by stimulating the alpha and beta 1 receptors.

B] Parasympathetic or Cholinergic receptors

1] Muscarinic receptor - when this receptor is stimulated, it causes a decrease in the heart rate, a decrease in heart contractility and a decrease in the size of the bronchioles. When we are at rest, we can
slow down and conserve energy.

2] Nicotinic receptors are involved in muscle contraction.

C] Agonist – neurotransmitters that interacts with and stimulates the receptors

1] When epinephrine or adrenaline is given to a patient, we expect alpha, beta 1 and beta 2 agonist effects such as Increase in blood pressure Increased heart rate, Increased cardiac contractility, Dilation of
the bronchioles in the lungs, Dilation of the vessels in the skeletal muscles.

2] Albuterol inhaler stimulates beta 2 receptors in the lungs that dilate the bronchioles in the patient with bronchospasm without causing excessive stimulation of the heart.

D] Antagonist - neurotransmitters that block the receptors which causes the opposite effect we would expect from stimulating the receptor.

1] Metoprolol blocks Beta 1 receptors thus decreasing heart rate and contractility which decreases blood pressure for the hypertensive patient and decreases the chance of a dysrhythmia after a heart attack
by controlling the heart rate.

2] Succinlycholine block the nicotinic receptors and induce paralysis necessary for certain medical procedures.

3] Atropine is a parasympatholytic antagonist used to counteract too much parasympathetic activity

4] Ipratroprium is a parasympathetic antagonist medication, which cause the bronchioles to dilate and decrease production of secretions like mucus.

5] If alpha-receptors are blocked, the arteries dilate. Thus an alpha-blocker medication such as prazosine causes vasodilation and can be used to treat hypertension.
Norepinephrine (NEl is synthesized in the nerve terminal through a series of steps that require the amino acids phenylalanine and tyrosine. The final step of the synthesis involves the conversion of dopamine
to norepinephrine.

The action of epinephrine is terminated through hepatic metabolism, rather than reuptake. Acetylcholine is synthesized in the presynaptic nerve tt'rminal from choline and acetyl coenzyme A

Stimulation of the sympathetic IIUVOU5 system: These drugs are called adrenergic agents or syrnpathomimrtia, and tht'y produce the classic symptoms of the fight-orflight response. Natural or synthetic
agents that produce a sympathomimetic response include the catecholamines and lIoncatecholamine;. 2. Inhibition of the sympathetic nervous system: These drugs are called adrenergic-blocking agents or
adrenergit antigonilts, and they produce actions opposite those of the sympathomimetics. The term syrnpatholytiu is another name for adrenergic antagonists.

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J.Stimularion of the parasympathetic nervous system: These drugs are called cholinergic agents or parasympathomimetics, and they produce the characteristic symptoms of the rest-and-digest response. 4.
Inhibition of the parasympathetic nervous system: These drugs are called cholinergic-blocking agents, ilntidtolinergics, parasympatholytics, or muscarinic blockers, and they produce actions opposite those of
the cholinergic agents.