Receptor-mediated inotropic drugs
1Division of Pharmacotherapy, Faculty of Medicine, University of Amsterdam, The Netherlands.
European Heart Journal
|June 1, 1988
Summary
This study reviews inotropic drugs that target cardiac adrenoreceptors and dopaminergic receptors. It discusses their receptor profiles and effectiveness in treating congestive heart failure.
Area of Science:
- Cardiovascular Pharmacology
- Adrenergic and Dopaminergic Receptor Signaling
Background:
- Cardiac inotropic activity is modulated by beta-1, beta-2, and alpha-1 adrenoreceptors.
- Dopaminergic receptor agonists offer limited direct inotropic effects but promote beneficial cardiovascular effects like vasodilation and improved renal perfusion.
Purpose of the Study:
- To survey cardiac beta- and alpha-adrenoreceptors and cardiovascular dopaminergic receptors.
- To discuss receptor-mediated inotropic drugs for congestive heart failure treatment.
Main Methods:
- Review of existing literature on adrenergic and dopaminergic receptor agonists.
- Analysis of receptor profiles and clinical applications of specific inotropic agents.
Main Results:
- Identified key inotropic drugs including isoprenaline, dobutamine, dopamine, and dopexamine.
- Detailed the receptor interactions and therapeutic scope of each drug.
Conclusions:
- Inotropic drugs targeting specific receptors offer therapeutic potential in congestive heart failure.
- Understanding receptor profiles is crucial for optimizing the use and limitations of these agents.
More Related Videos
Related Concept Videos
Heart Failure Drugs: Inotropic Agents
1.6K
Positive inotropic agents are commonly used as the first line of treatment for heart failure. One such agent is digoxin, derived from the genus Digitalis, which has been known for centuries but effectively utilized since 1785. However, these cardiac glycosides can have potentially toxic effects due to their mechanism of action, which involves inhibiting Na+/K+-ATPase and increasing contractility. Digoxin is absorbed orally and distributed in various tissues, including the CNS. It has a long...
1.6K
Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers
2.1K
Adrenergic stimulation generally impacts cardiac rate and rhythm. Specifically, stimulation of the β-adrenoceptors triggers an increase in intracellular calcium ion influx and pacemaker currents, which may cause arrhythmias. Catecholamines like adrenaline also demonstrate β2-adrenoceptor-mediated hypokalemia, impacting cardiac action potential and disrupting the normal cardiac rhythm. Class II antiarrhythmic drugs are β-adrenoceptor antagonists or β-blockers, which...
2.1K
Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers
2.6K
Class III antiarrhythmic drugs are a group of medications that can prolong action potentials in the heart. They achieve this by blocking potassium channels or enhancing inward currents from sodium channels. However, these drugs have a unique property of "reverse use-dependence," which is most pronounced at slower heart rates and can lead to torsades de pointes—a specific type of arrhythmia. However, it is essential to note that excessive QT interval prolongation—a measure of...
2.6K
Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers
3.6K
Class I antiarrhythmic drugs are used to treat various types of arrhythmias or irregular heart rhythms. These drugs block the sodium (Na+) channels in the cardiac cells, thereby affecting the movement of electrical impulses across the heart. Class I antiarrhythmic drugs are divided into three subgroups: Class IA, Class IB, and Class IC, each with distinct mechanisms of action and effects on the heart.
Class 1A Antiarrhythmic Drugs: These drugs work by moderately blocking sodium channels,...
Class 1A Antiarrhythmic Drugs: These drugs work by moderately blocking sodium channels,...
3.6K
Antiarrhythmic Drugs: Class IV Agents as Calcium Channel Blockers
2.3K
Class IV antiarrhythmic drugs, such as verapamil and diltiazem, block calcium channels. They primarily affect the heart, slowing the conduction in calcium-dependent tissues like the SA and AV nodes. These drugs manage reentrant supraventricular tachycardia (SVT) and reduce ventricular rate in atrial flutter/fibrillation.
Verapamil, a calcium channel blocker, inhibits calcium movement across myocardial cell membranes and vascular smooth muscle. This results in the dilation of coronary and...
Verapamil, a calcium channel blocker, inhibits calcium movement across myocardial cell membranes and vascular smooth muscle. This results in the dilation of coronary and...
2.3K
Adrenergic Agonists: Indirect-Acting Agents
2.8K
Indirect-acting adrenergic agonists potentiate the effects of endogenous catecholamines through different mechanisms without directly binding to adrenoceptors.
One mechanism involves depleting stored catecholamines by displacing them from synaptic vesicles. These agents, known as "displacers," are transported into vesicles at the expense of noradrenaline. Examples include amphetamine and tyramine, which lack a catechol moiety, resulting in prolonged action, improved oral...
One mechanism involves depleting stored catecholamines by displacing them from synaptic vesicles. These agents, known as "displacers," are transported into vesicles at the expense of noradrenaline. Examples include amphetamine and tyramine, which lack a catechol moiety, resulting in prolonged action, improved oral...
2.8K


