Nervous System part 1

 

Autonomic Nervous System   Physiology Review: • Activities are not under direct conscious control • Responsible for cardiac and smooth muscle (e.g., respiratory tract) activity, digestion as well as glandular secretion • Divided into: • Sympathetic System • Activated under conditions of stress (“fight or flight”) • Parasympathetic System • Activated under nonstressful conditions (“rest and digest

Autonomic Nervous System Effects Sympathetic (SNS) Parasympathetic (PNS) Pupils Dilates Constricts Tear glands No effect Stimulates Salivary stimulation Inhibits Stimulates Heart rate Increases Decreases Arterioles Constricts Dilates Bronchi Dilation Constricts GI motility Inhibits Stimulates Pancreas Inhibits Stimulates Bladder Relaxes Contracts Erection/Ejaculation Stimulates ejaculation Stimulates erection

Major Neurotransmitters of the Autonomic Nervous System • Released by Sympathetic Nervous System: • Norepinephrine (NE) • Epinephrine (Epi) • Released by Parasympathetic Nervous System: • Acetylcholine (Ach) • Key Pharmacological Implications: • Agents that increase NT release • Agents that decrease NT degradation • Receptor agonists and/or antagonists

Autonomic Nervous System (ANS) =Sympathetic Nervous System (SNS) +Parasympathetic Nervous System (PNS)

Sympathetic Nervous System (SNS) Major Mediators • Catecholamines: • Metabolized by catechol-O-methyltransferase (COMT) and monoamine oxidase (MAO) • Epinephrine (Epi) and Norepinephrine (NE) • Sympathomimetic • Sympathetic agonists (similar to Epi or NE) • Sympatholytic • Sympathetic antagonist (blocks the effects of Epi or NE) • Dopamine (DA): • Endogenous NT with sympathetic characteristics • Works at DA, α and β1 receptor sites

Stimulation of SNS Receptors Receptor Select Agonist Action and Uses Stimulation Effects α1 • Smooth muscle contraction • Mydriasis during eye exams • Treatment of: • Nasal congestion • Hypotension • Vasoconstriction • Pupil dilation • ↓ Secretions • ↓ GI motility α2 • Smooth muscle contraction + NT inhibition • Treatment of hypertension (activation of receptors reduces the release of NE) • ↓ CNS sympathetic outflow • ↓ NE release • ↓ Insulin release

Stimulation of SNS Receptors Receptor Select Agonist Action and Uses Stimulation Effects β1 • Heart muscle contraction • Treatment of: • Cardiac arrest • Heart failure • Shock • ↑ Heart rate • ↑ Cardiac output (CO) • ↑ Stroke volume (SV) • ↑ Cardiac automaticity • ↑ Cardiac contractility • ↑ Renin secretion β2 • Smooth muscle relaxation • Treatment of: • Asthma • Premature contractions of labor • Bronchial relaxation • Uterine relaxation • Vasodilation to skeletal muscle vessels

Adrenergic Agents (Sympathomimetics) Select Examples Receptor Subtype Major Uses Albuterol (Proventil; Ventolin) β2 • Asthma Isoproterenol (Isuprel) β1: (↑ heart rate, ↑ contractility) β2: (vasodilation, bronchodilation) • Asthma • Dysrhythmias • Heart failure Salmeterol (Serevent) β2 • Asthma Terbutaline (Brethine) β2 • Asthma • Slow uterine contractions Epinephrine (Adrenalin) α & β • Cardiac arrest (↑ heart rate) • Anaphylaxis (bronchodilation)

Adrenergic Agents (Sympathomimetics - continued) Select Examples Receptor Subtype Major Uses Dobutamine (Dobutrex) β1 • Cardiac Stimulant Clonidine (Catapres) α2 in CNS • Hypertension Oxymetazoline (Afrin) α • Nasal congestion Pseudoephedrine (Sudafed) α > β • Nasal congestion Dopamine (Intropin) α1 & β1 • Shock Norepinephrine (Levophed) α > β1 • Shock (vasoconstriction and ↑ heart rate) Phenylephrine (NeoSynephrine) α1 ,α2 • Shock (vasoconstriction; causes reflex bradycardia) • Nasal congestion

Adrenergic Blocking Agents (Sympatholytics/Sympathetic Antagonists) Select Examples Receptor Subtype Major Uses Atenolol (Tenormin) β1 specific* • Angina • Hypertension Timolol (Timoptic) Blocks β1 & β2 • Angina • Glaucoma (↓ intraocular pressure) • Hypertension Prazosin (Minipress) Blocks α1 • BPH • Hypertension Tamsulosin (Flomax) Blocks α1 • BPH

Physiology Review: • Classic parasympathomimetic: acetylcholine (Ach) • Acetylcholine will bind to 2 types of receptors: 1. Nicotinic (ganglia) 2. Muscarinic (organs) • After binding to and activating the receptor, Ach is broken down by the enzyme, acetylcholine esterase (AchE) • AChE metabolizes Ach into: • Choline • Acetate • Nerve terminals can then take choline and acetate and re-synthesize Ach • Parasympathetic effects = “cholinergic” effects