Related Experiment Video
Updated: Aug 11, 2026
08:41
Assessment of Vascular Tone Responsiveness using Isolated Mesenteric Arteries with a Focus on Modulation by Perivascular Adipose Tissues
Published on: June 3, 2019
Diazepam attenuates phenylephrine-induced contractions in rat aorta
Soon-Eun Park1, Ju-Tae Sohn, Cheol Kim
1Department of Anesthesiology and Pain Medicine, Ulsan University College of Medicine, Ulsan, Republic of Korea.
Anesthesia and Analgesia
|February 24, 2006
Summary
Diazepam, a common sedative, reduces phenylephrine-induced contractions in rat aorta by enhancing nitric oxide production. This effect involves both endothelial and direct vascular smooth muscle actions.
Area of Science:
- Pharmacology
- Cardiovascular Physiology
- Vascular Biology
Background:
- Diazepam is a benzodiazepine anxiolytic with known cardiovascular effects.
- Endothelium-derived vasodilators play a crucial role in regulating vascular tone.
- The precise vascular mechanisms of diazepam, particularly its interaction with endothelial factors, require further elucidation.
Purpose of the Study:
- To investigate the in vitro effects of diazepam on phenylephrine-induced contractions in rat aorta.
- To determine the cellular mechanisms underlying diazepam's actions, focusing on endothelium-derived vasodilators.
- To assess the influence of diazepam on nitric oxide and other vasoactive pathways.
Main Methods:
- In vitro study using isolated rat aortic rings.
- Generation of concentration-response curves for phenylephrine and potassium chloride in the presence and absence of diazepam.
- Pretreatment of aortic rings with N(W)-nitro-L-arginine methyl ester (L-NAME), PK 11195, tetraethylammonium, and indomethacin to probe specific pathways.
Main Results:
- Diazepam (7 x 10(-7) M) attenuated phenylephrine-induced contractions in endothelium-intact aortic rings.
- Higher diazepam concentrations (5 x 10(-6) M) attenuated contractions in aortic rings with or without endothelium.
- Pretreatment with L-NAME abolished diazepam-induced attenuation, indicating a role for nitric oxide.
- L-NAME-induced contraction was enhanced by diazepam, suggesting increased nitric oxide synthase activity.
Conclusions:
- Supraclinical concentrations of diazepam attenuate phenylephrine-induced contractions in rat aorta.
- The primary mechanism involves the enhancement of endothelial nitric oxide production.
- Diazepam also exerts direct effects on vascular smooth muscle, contributing to vasodilation.
More Related Videos
Related Concept Videos
01:23Antihypertensive Drugs: Vasodilators
Vasodilators, primarily affecting the smooth muscles within arterial and venous walls, are commonly used for hypertension treatment. Medications such as minoxidil and hydralazine primarily target arteries and arterioles, while sodium nitroprusside acts on arterioles and venules. Minoxidil, functioning as a prodrug, is metabolized by hepatic sulfotransferase into its active form, minoxidil sulfate, after oral administration. This metabolite binds to the sulfonylurea receptor (SUR) component of...
01:18Antihypertensive Drugs: Action of Calcium Channel Blockers
Calcium ions are essential to contract smooth muscle cells in blood vessels. They enter these cells through voltage-dependent calcium channels, specifically L-type calcium channels in the cell membrane. These L-type calcium channels are integral to the excitation-contraction coupling process in smooth muscle. When a stimulus is received by smooth muscle cells, their membrane depolarizes. This alteration in membrane potential instigates the opening of L-type calcium channels. As a result,...
01:31Adrenergic Antagonists: ɑ and β-Receptor Blockers
Third-generation β-blockers, such as labetalol and carvedilol, represent a significant advancement in managing cardiovascular conditions. Unlike conventional β-blockers, which can induce peripheral vasoconstriction, third-generation drugs block α1 adrenoceptors. This promotes vasodilation through several mechanisms, such as increased nitric oxide production, inhibition of calcium ion entry, opening of potassium ion channels, and antioxidant action. Labetalol, for instance, is clinically...
01:22Heart Failure Drugs: β-Blockers
β-adrenergic antagonists, commonly known as β-blockers, block the effects of sympathetic neurotransmitters such as noradrenaline (NA) and adrenaline (ADR). They have several beneficial effects in heart failure treatment. They reduce heart rate, the force of contraction, and cardiac muscle relaxation. They also slow the atrial-ventricular conduction rate and raise the threshold for arrhythmias. The concentration of β-blockers determines their effects on bronchodilation, vasodilation, and...
01:20Antiarrhythmic Drugs: Class IV Agents as Calcium Channel Blockers
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...
01:25Antianginal Drugs: Calcium Channel Blockers and Ranolazine
Angina pectoris, a primary symptom of ischemic heart disease, requires careful pharmacological interventions. In this context, calcium channel blockers (CCBs) and ranolazine have emerged as crucial pharmacotherapeutic agents, providing deep insights into the complexities of angina management.
CCBs, a diverse class that includes dihydropyridines (nifedipine) and diphenylalkylamines (verapamil and diltiazem), exert their effect by blocking calcium channels in cardiac and smooth muscle cells. This...
CCBs, a diverse class that includes dihydropyridines (nifedipine) and diphenylalkylamines (verapamil and diltiazem), exert their effect by blocking calcium channels in cardiac and smooth muscle cells. This...