Autonomic Nervous System - Pharmacology

The autonomic nervous system also known as the visceral system involuntarily regulates smooth muscles and glands including the heart, respiratory system, GI tract, peristalsis (digestion), bladder, and eyes.

The autonomic nervous system has two sets of nerves. These are the sensory neurons (afferent) and the motor neurons (efferent). Sensory neurons send impulses to the central nervous system, which are transmitted to the brain where they are interpreted. The brain then sends a response to the motor neuron’s brain through the spinal cord that directs specific organ cells to respond to the sensory neuron’s impulse.

Previously in this chapter you learned that the autonomic nervous system has two branches. These are the sympathetic branch and parasympathetic branch. Both branches act on the same organ cells but in an opposite way. The sympathetic branch stimulates a response and the parasympathetic branch depresses a response by the organ cell. Together, they keep the organ in balance (homeostasis).

The sympathetic branch stimulates a response using nor epinephrine, a neurotransmitter. Medications that mimic the effect of nor epinephrine are called adrenergic drugs or sympathomimetics (mimic sympathetic nervous system actions) (see chart). These drugs are also known as adrenergic agonists because they start a response at the adrenergic receptor sites. There are four types of adrenergic receptors. These are alpha1, alpha2, beta1, and beta2. (see chart)

The parasympathetic branch depresses a response using adrenergic blockers also known as sympatholytics. Lytic means to stop effect. Adrenergic blockers prevent the norepinephrine response at the adrenergic receptor sites.

The parasympathetic branch is sometimes referred to as the cholinergic system because an acetylcholine neurotransmitter is used to innervate muscle cells at the end of the neuron. Acetylcholine stimulates receptor cells to produce a

Physiologic-responses

response. However, the enzyme acetylcholinesterase can inactivate the acetyl-choline before it reaches the receptor cell.

Drugs that mimic acetylcholine are cholinergic agonists because they initiate a response. These are also known as cholinergic drugs or parasympathomimetics (see chart).

Drugs that block the effect of acetylcholine are called anticholinergic, or parasympatholytics. They are also known as cholinergic antagonists because they inhibit the effect of acetylcholine on the organ.

There are two types of cholinergic receptors. These are nicotinic or muscarinic. Nicotinic receptors are stimulated by alkaloids nicotine. Muscarinic receptors are stimulated by muscarine.

Sympathetic--Parasympathetic--Stimulants

Sympathetic--Parasympathetic--Depressants

THE FIGHT OR FLIGHT RESPONSE

Norepinephrine and acetylcholine neurotransmitters produce a fight or flight response (see chart). In a fight response, eyes dilate so you can see better and lungs inspire more oxygen while increasing your heart rate. Blood vessels con-strict increasing blood pressure. Smooth muscles along the bladder and the GI tract relax so that energy is not expended on digestion. Salivary glands reduce the secretion of saliva giving the person the dry mouth feeling in an emergency. The flight response is really a misnomer because it doesn’t help you run away. Instead, the flight response is really the opposite of fight and allows the individual to relax and function normally. In the flight response or the non-fight mode, pupils constrict, the heart rate slows, the GI tract reduces function, and breathing slows down.

THE FIGHT OR FLIGHT RESPONSE

ADRENERGICS AND ADRENERGIC BLOCKERS

Andrenergics are medications that stimulate alpha1-receptors and beta-adren-ergic receptors. Alpha1-receptors are located in the smooth muscle of vascular (vessels) tissues. Beta-adrenergic receptors are in the smooth muscle of the lungs, arterioles of skeletal muscles, and the uterine muscles. Adrenergics also stimulate the dopaminergic receptor located in the renal, mesenteric, coronary, and cerebral arteries to dilate and increase blood flow. Dopamine is the only adrenergic that can activate this receptor.

Adrenergic blockers inactivate these receptors in three ways:

  1. They promote reuptake of the transmitter back into the neuron (nerve cell terminal).
  2. Transmitters are transformed or degraded by enzymes making them unable to attach to a receptor. Two enzymes that inactive norepinephrine are monoamine oxidase (MAO) and catechol-o-methyl-transferase (COMIT). MAO is inside the neuron and COMIT is outside the neuron.
  3. Transmitters are diffused away from receptors.

Sympathomimetic drugs stimulate andrenergic receptors and are classified into three categories according to its effect on organ cells. These categories are:

  1. Direct-acting sympathomimetics-directly stimulate receptors.
  2. Indirect-acting sympathomimetics-stimulate the release of norepinephrine from terminal nerve endings.
  3. Mixed-acting sympathomimetics-have the effect of both direct-acting sympathomimetics and indirect-acting sympathomimetics. They simulate the adrenergic receptor sites and stimulate the release of norepinephrine from terminal nerve endings. Ephedrine is an example of a mixed-acting sympathomimetic and is used to treat idiopathic orthostatic hypotension and hypotension resulting from spinal anesthesia. Ephedrine also stimulates beta2-receptors to dilate bronchial tubes and is used treat mild forms of bronchial asthma.

Many adrenergic medications stimulate more that one adrenergic receptor site. For example, epinephrine (Adrenalin) acts on alpha1 -, beta1 -, beta2-receptor sites. These receptor sites include an increase in blood pressure, pupil dilation, increase in heart rate (tachycardia), and bronchodilation.

Epinephrine (Adrenalin) is used to treat cardiogenic and anaphylactic shock because it increases blood pressure, heart rate, and airflow through the lungsthrough bronchodilation. Because it affects three different receptors, it lacks selectivity.

Alpha-adrenergic blockers inhibit the response at the alpha-adrenergic receptor sites. There are two types of alpha-adrenergic blockers: selective and nonse-lective blockers. Both types decrease symptoms of benign prostatic hypertrophy (BPH) (enlarged prostate) and promote vasodilation and treat peripheral vascular disease such as Raynaud’s disease. Doxazosin (Cardura) is a selective alpha1-blocker and phentolamine (Regitine) is a nonselective alpha adrenergic blocker. Both can be used to treat hypertension.

However, alpha-adrenergic blockers can cause orthostatic hypotension (drop in blood pressure when an individual stands up), dizziness, and reflex tachycardia. They are not as frequently prescribed as beta-blockers.

Beta-adrenergic blockers (see chart)also known beta blockersdecrease heart rate and decrease blood pressure resulting in bronchoconstriction. Therefore, beta-adrenergic blockers should be used with caution for patient’s who have COPD or asthma.

Other-Adrenergics

There are also two types of beta-adrenergic blockers: selective and non-selective. For example, metoprolol tartrate (Lopressor) is a selective beta-adrenergic blocker that blocks beta, receptors to decrease pulse rate and decreaseblood pressure. Propranolol NCl (Inderal) is a non-selective beta-adrenergic blocker that blocks both beta1 and beta2 receptors resulting in a slower heart rate, decreased cardiac output, and lower blood pressure.

Other-Beta-Blockers

Selective-Beta-Adrenergics


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