We can also stimulate a single receptor site such as a beta-2 agonist medication like an albuterol inhaler that stimulates beta-2 receptors in the lungs then we can dilate the bronchioles in the patient with bronchospasm without causing excessive stimulation of the heart. The sympathetic receptors can be over-stimulated by the non-therapeutic use of substances like cocaine and methamphetamines. Or the excessive use or overdose of sympathomimetic medication like pseudoephedrine or those used to treat attention deficit disorders.
Severe alcohol withdrawal may also induce sympathetic overdrive. Excessive stimulation of the sympathetic receptors can result in dangerously high blood pressure, tachycardia, dysrhythmias and hyperthermia, any one of which may cause organ damage with the real potential for organism death. Now let's switch to the parasympathetic or cholinergic receptors.
These are easier since there are only two types, muscarinic receptors and nicotinic receptors. And I will make it even easier by getting rid of the nicotinic receptors after I tell you they are involved in muscle contraction and are affected by substances such as curare used on those poison-tipped arrows that cause muscle paralysis by blocking these nicotinic receptors.
Medications such as succinlycholine are available to block the nicotinic receptors and induce paralysis necessary for certain medical procedures. We are left with the one parasympathetic receptor you must learn, the 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. The parasympathetic nervous system helps us do this. What would happen if we block the muscarinic receptors?
That would cause the heart rate and contractility to increase, dilation of the bronchioles and less production of secretions in the body. This is the exact effect of atropine, a drug we use to counteract too much parasympathetic activity such as from over-stimulation of the vagus nerve or the effects of certain chemical warfare nerve agents and organophosphate poisoning. Atropine is a parasympatholytic, we can also call it a parasympathetic antagonist or parasympathetic blocker or an anticholinergic medication.
All these terms mean the same; it means they block the action of acetylcholine at the parasympathetic receptors. The effect of blocking any receptor causes the opposite effect we would expect from stimulating the receptor. Ipratroprium is another example of a parasympathetic blocker medication but this one is inhaled so most of the effect occurs in the lungs, and when we block parasympathetic receptors in the lungs we cause the bronchioles to dilate and decrease production of secretions like mucus.
That makes ipratroprium useful in the patient with COPD who produces excessive pulmonary mucous and in combination with albuterol for any wheezing patient. But remember that the primary rescue medication for bronchospasm is a beta 2 agoinist such as albuterol although ipratrorium is often added and is available as a combination inhaler with albuterol called Combivent.
It is important to remember that it is the balance between the sympathetic and parasympathetic nervous system that keeps our automated body functions in balance and working properly. Outside forces, including drugs, medications or poisons can change the functioning of the autonomic nervous system. Dopamine and dobutamine activate the myocardial beta 1 receptor and thus increase the force of contraction of the failing heart.
This will result in an increase in cardiac output. These drugs are reserved for use in the acute management of heart failure. These agents have a higher affinity lower equilibrium dissociation constant for beta 2 receptors when compared to beta 1. Therefore, they selectively activate beta 2 receptors when compared to beta 1. Uses 1. Airways dysfunction; bronchial asthma, chronic bronchitis, emphysema In airways dysfunction, beta 2 selective agonists relax airways thus decreasing airways resistance.
Premature labor In premature labor, the beta 2 selective agonists relax uterine smooth muscle. Drugs that relax uterine smooth muscle are referred to as tocolytic agents. Side effects related to dental practice 1. Xerostomia, with inhaler usage.
These structural modifications of the parent catecholamine nucleus result in drugs that are orally active and have longer plasma half-lives. However, these same modifications result in lower affinity for the receptor than do the endogenous agonists epinephrine or norepinephrine.
There are two structural classes of alpha 1 agonists phenethylamines which are closely aligned in structure to epinephrine and the imidazolines, compounds structurally unrelated to epinephrine. Levonordeferin is a phenyethylamine that has been used in dental practice in combination with local anesthetics.
Hypotension-to increase blood pressure during a surgical procedure where a general anesthetic has induced hypotension 2. Ophthalmic preparations-to induce mydrasis also in topical preparations for symptomatic release of eye irritation.
Cough and cold preparations-Induces constriction of nasal mucosa decreases resistance to air flow. Indirect Acting Sympathomimetics These agents require the presence of endogenous catecholamines to produce their effects.
They have little activity if catecholamines are depleted. Cocaine: Blocks reuptake of monoamines into nerve endings. Cocaine also has local anesthetic activity. Amphetamine: Promotes the release of NE from nerve endings. Amphetamine can also block the reuptake of norepinephrine. Amphetamine-like compounds 1. Methylphenidate A major site action of cocaine, amphetamine and amphetamine-like agents is in the CNS.
These drugs produce a feeling of well being and euphoria. As a result the drugs carry a significant abuse liability. Both cocaine and amphetamine are on the FDA schedule 2. Uses of Cocaine 1 below , Amphetamine and Amphetamine-like agents below 1. Cocaine has limited use as a local anesthesic and vasoconstrictor in surgical procedures involving oral, laryngeal or nasal cavities.
Appetite suppression 3. Hyperactivity in children 4. Recall that epinephrine can be absorbed systemically after intraoral administration. This epinephrine can be taken up by nerve terminals and this uptake contributes to the the termination of the actions of epinephrine. Thus, the risk of hypertension and other problems associated with systemic absorption of epinephrine will be greater in patients taking cocaine or amphetamine-like drugs.
Methamphetamine can be produced from over the counter cough and cold medications such as pseudoephedrine. Lithium, muriatic acid, sulfuric acid, red phosphorus and lye are used in this preparation.
When smoked these highly corrosive agents are vaporized resulting in significant damage to teeth and gums. Sympatholytics: synthetic analogs which bind to beta or alpha receptors or act through other mechanisms to block the actions of endogenous neurotransmitters or other sympathomimetics. Review the pharmacodynamic properties and characteristics of antagonists.
Understand the pharmacologic properties and therapeutic uses of clonidine, prazosin analogs, the beta blockers and MAO-inhibitors. Understand the special precautions that exist for sympatholytic drugs in dental practice. This drug stimulates alpha 2 receptors in the nucleus tractus solitarius NTS to decrease sympathetic outflow to the heart and blood vessels.
The decrease in sympathetic tone results in a decrease in peripheral vascular resistance. Clonidine is used in dental practice in the management of chronic pain. It can be given orally or in patch form.
Clonidine is a second-line antihypertensive that has many other uses including opiate withdrawal, nicotine withdrawal, vascular headaches, diabetic diarrhea, glaucoma, ulcerative colitis and Tourette's syndrome. Side Effects The use of clonidine may result in clinical symptoms related to dry mouth, such as difficulty in swallowing and speech.
Chronic use of xerostomia-producing drugs is associated with a higher incidence of oral candidiasis and dental caries. Epinephrine 10 nM , a concentration causing maximum increase in contractile force, and norepinephrine 1 and microM increased cAMP-dependent protein kinase activity in TG4 left ventricle.
Cardiodepressive concentrations of epinephrine 1 and microM did not increase cAMP-dependent protein kinase activity. The inotropic results were simulated with a model of two beta 2 -adrenoceptor sites. For one site involved in receptor coupling to G s , both epinephrine and norepinephrine compete.
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