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Skip Navigation. FASTtrack: Pharmacology. FASTtrack: Pharmacology is a study guide providing an account of drug action, as well as dealing with molecular pharmacology at a more advanced level. New in this edition: Each chapter completely updated to take account of recent changes, and include future drugs Multiple choice tests New chapters on immunopharmacology, oral contraceptives and local anaesthetics Greater use of summary tables. Pharmacodynamics 2. Receptors 3.

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G-proteins and Their Downstream Signaling Cascades 4. Ion Channels and Transporters 5. Quantitive Pharmacology 6. Autonomic Pharmacology 7. Local Mediators 8. Pharmacokinetics and Drug Metabolism 9. Gastric Pharmacology Lower Gastrointestinal Pharmacology Antiemetics Antiarrhythmics Cardiovascular Drugs Renal and Urinary Pharmacology Antithrombotic Agents Antiobesity Drugs Asthma and Chronic Obstructive Pulmonary Disease Allergy Anxiolytics and Hypnotics Antidepressants Antiepileptic Drugs Antipsychotic Drugs Parkinson's Disease Analgesics Drugs of Abuse General Anaesthetics Neuromuscular Blocking Drugs Thyroid Disorders Finally, PK-A can phosphorylate myosin light chains, which may contribute to the positive inotropic effect of beta-adrenoceptor stimulation.

Because there is generally some level of sympathetic tone on the heart, beta-blockers are able to reduce sympathetic influences that normally stimulate chronotropy heart rate , inotropy contractility , dromotropy electrical conduction and lusitropy relaxation. Therefore, beta-blockers cause decreases in heart rate, contractility, conduction velocity, and relaxation rate. These drugs have an even greater effect when there is elevated sympathetic activity.

These receptors, like those in the heart, are coupled to a Gs-protein , which stimulates the formation of cAMP. Although increased cAMP enhances cardiac myocyte contraction see above , in vascular smooth muscle an increase in cAMP leads to smooth muscle relaxation. The reason for this is that cAMP inhibits myosin light chain kinase that is responsible for phosphorylating smooth muscle myosin.

Beta-blockers are used for treating hypertension, angina, myocardial infarction, arrhythmias and heart failure. Beta-blockers decrease arterial blood pressure by reducing cardiac output.

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Many forms of hypertension are associated with an increase in blood volume and cardiac output. Therefore, reducing cardiac output by beta-blockade can be an effective treatment for hypertension, especially when used in conjunction with a diuretic. Acute treatment with a beta-blocker is not very effective in reducing arterial pressure because of a compensatory increase in systemic vascular resistance. Chronic treatment with beta-blockers lowers arterial pressure more than acute treatment possibly because of reduced renin release and effects of beta-blockade on central and peripheral nervous systems.

Decreasing circulating plasma renin leads to a decrease in angiotensin II and aldosterone , which enhances renal loss of sodium and water and further diminishes arterial pressure.


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Hypertension in some patients is caused by emotional stress, which causes enhanced sympathetic activity. Beta-blockers can be very effective in these patients. Beta-blockers are used in the preoperative management of hypertension caused by a pheochromocytoma, which results in elevated circulating catecholamines. When used for this condition, the blood pressure is first controlled using an alpha-blocker such as phenoxybenzamine , and then a beta-blocker can be carefully administered to reduce the excessive cardiac stimulation by the catecholamines. It is important that a beta-blocker is administered only after adequate blockade of vascular alpha-adrenoceptors so that a hypertensive crisis does not occur as a result of unopposed alpha-adrenoceptor stimulation.

The antianginal effects of beta-blockers are attributed to their cardiodepressant and hypotensive actions. By reducing heart rate, contractility, and arterial pressure, beta-blockers reduce the work of the heart and the oxygen demand of the heart.

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Furthermore, beta-blockers have been found to be very important in the treatment of myocardial infarction in that they have been shown to decrease mortality. The antiarrhythmic properties beta-blockers Class II antiarrhythmic are related to their ability to inhibit sympathetic influences on cardiac electrical activity.

Sympathetic nerves increase sinoatrial node automaticity by increasing the pacemaker currents, which increases sinus rate. Sympathetic activation also increases conduction velocity particularly at the atrioventricular node , and stimulates aberrant pacemaker activity ectopic foci.

Therefore, beta-blockers can attenuate these sympathetic effects and thereby decrease sinus rate, decrease conduction velocity which can block reentry mechanisms , and inhibit aberrant pacemaker activity. Beta-blockers also affect non-pacemaker action potentials by increasing action potential duration and the effective refractory period.

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This effect can play a major role in blocking arrhythmias caused by reentry. The majority of patients in heart failure have a form that is called systolic dysfunction , which means that the contractile function of the heart is depressed loss of inotropy. Although it seems counterintuitive that cardioinhibitory drugs such as beta-blockers would be used in cases of systolic dysfunction, clinical studies have shown quite conclusively that some specific beta-blockers actually improve cardiac function and reduce mortality. Furthermore, they have been shown to reduce deleterious cardiac remodeling that occurs in chronic heart failure.

Although the exact mechanism by which beta-blockers confer their benefit to heart failure patients is poorly understood, it may be related to blockade of excessive, chronic sympathetic influences on the heart, which are known to be harmful to the failing heart.

Some beta-blockers have additional mechanisms besides beta-blockade that contribute to their unique pharmacologic profile. The two classes of beta-blockers along with specific compounds are listed in the following table. Additional details for each drug may be found at www.