Related Experiment Video
Updated: May 29, 2026
05:24
Surgical Lumbar Sympathectomy in Mice
Published on: July 5, 2024
Central sympatholytic drugs
Wanpen Vongpatanasin1, Kazuomi Kario, Steven A Atlas
1Hypertension Section, University of Texas Southwestern Medical Center, Dallas, TX, USA. wanpen.vongpatanasin@utsouthwestern.edu
Journal of Clinical Hypertension (Greenwich, Conn.)
|September 8, 2011
Summary
Central sympatholytic drugs lower blood pressure by acting on the brainstem, but their use is limited by side effects and the risk of rebound hypertension. These medications are typically reserved for resistant hypertension cases.
Area of Science:
- Pharmacology
- Cardiovascular Medicine
- Neuroscience
Background:
- Central sympatholytic drugs, such as centrally acting alpha-2 adrenergic agonists, represent a class of antihypertensive agents.
- These medications exert their effects by modulating the sympathetic nervous system centrally within the brainstem.
Purpose of the Study:
- To elucidate the mechanism of action of central sympatholytic drugs.
- To discuss the current clinical positioning and limitations of these agents in hypertension management.
- To highlight potential adverse effects and contraindications for their use.
Main Methods:
- Review of existing pharmacological and clinical literature on central sympatholytic agents.
- Analysis of the neurochemical pathways involved in sympathetic regulation.
- Evaluation of clinical trial data and practice guidelines regarding their efficacy and safety.
Main Results:
- Central sympatholytic drugs reduce blood pressure by stimulating central alpha(2)-adrenergic receptors, decreasing sympathetic outflow.
- Common side effects include drowsiness, fatigue, and dry mouth, limiting their use.
- Rebound hypertension is a significant concern, especially with short-acting agents and in non-adherent patients.
Conclusions:
- Central sympatholytic drugs are effective antihypertensives but are generally considered fourth-line or later due to side effect profiles.
- Their use should be carefully considered, avoiding "as needed" administration for asymptomatic blood pressure surges due to rebound risk.
- Patient adherence and drug half-life are critical factors in managing potential adverse outcomes.
Related Concept Videos
01:30Adrenergic Agonists: Direct-Acting Agents
Drugs that mimic the action of endogenous catecholamines like noradrenaline and adrenaline are called adrenergic agonists or sympathomimetics. Based on their mechanism of action, sympathomimetics can be classified as direct-, indirect-, or mixed-acting sympathomimetics. Direct-acting adrenergic agonists activate adrenoceptors without affecting presynaptic neurons, making them independent of neuronal catecholamine-depleting agents like reserpine and guanethidine.
These agents can be classified...
These agents can be classified...
01:30Adrenergic Agonists: Therapeutic Uses
Adrenergic agonists have diverse therapeutic uses across various medical conditions and emergencies.
Emergency and Intensive Care Unit (ICU) applications: Pressor agents increase blood pressure, heart rate, and contractility in shock and organ failure situations. Dopamine can induce vasodilation and stimulate adrenoceptors. Endogenous catecholamines are effective in treating cardiogenic shock. α2-agonists like clonidine can reverse anesthesia-induced hypertension.
Allergies and anaphylaxis:...
Emergency and Intensive Care Unit (ICU) applications: Pressor agents increase blood pressure, heart rate, and contractility in shock and organ failure situations. Dopamine can induce vasodilation and stimulate adrenoceptors. Endogenous catecholamines are effective in treating cardiogenic shock. α2-agonists like clonidine can reverse anesthesia-induced hypertension.
Allergies and anaphylaxis:...
01:18Adrenergic Agonists: Therapeutic Classification
Adrenergic agonists can be classified based on their therapeutic uses and mechanisms of action. They serve various purposes in clinical applications.
Vasopressor or pressor agents: They increase blood pressure and function as cardiac stimulants. Examples include endogenous catecholamines (norepinephrine and dopamine) and synthetic agents (phenylephrine).
Bronchodilators: β2-agonists can relax bronchial muscles and widen airways. They are commonly used for treating obstructive pulmonary...
Vasopressor or pressor agents: They increase blood pressure and function as cardiac stimulants. Examples include endogenous catecholamines (norepinephrine and dopamine) and synthetic agents (phenylephrine).
Bronchodilators: β2-agonists can relax bronchial muscles and widen airways. They are commonly used for treating obstructive pulmonary...
01:28Drugs Acting on Autonomic Ganglia: Blockers
Ganglionic blockers inhibit autonomic activity by blocking nicotinic receptors in the autonomic ganglia, suppressing impulse transmission. These blockers lack selectivity between sympathetic and parasympathetic ganglia and are ineffective as neuromuscular junction antagonists. They can be categorized into two groups:
01:16Antianginal Drugs: Nitrates and β-Blockers
In cardiovascular health, antianginal drugs combat angina pectoris — a condition marked by chest pain owing to diminished blood flow to the heart.
Organic nitrates, such as nitroglycerin, play a pivotal role. Once metabolized, they liberate nitric oxide, a molecular marvel. Nitric oxide triggers guanylyl cyclase and augments cGMP production. This biochemical cascade orchestrates the relaxation of vascular smooth muscles, ushering in vasodilation and enhancing coronary blood flow. Administered...
Organic nitrates, such as nitroglycerin, play a pivotal role. Once metabolized, they liberate nitric oxide, a molecular marvel. Nitric oxide triggers guanylyl cyclase and augments cGMP production. This biochemical cascade orchestrates the relaxation of vascular smooth muscles, ushering in vasodilation and enhancing coronary blood flow. Administered...
01:25Adrenergic Agonists: Indirect-Acting Agents
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 bioavailability, and...
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 bioavailability, and...