Differential effects of calcium-channel blockers on vascular endothelial function in patients with coronary spastic

Yoichi Miwa1, Hiroyuki Masai, Masatoshi Shimizu

  • 1Department of Internal Medicine, National Hospital Organization Kobe Medical Center, Kobe, Japan. yomiwa-circ@umin.ac.jp

Insights

Benidipine improved endothelial function in coronary vasospasm patients, unlike diltiazem or verapamil. This suggests dihydropyridine calcium-channel blockers may benefit vascular endothelial function.

Area of Science:

  • Cardiovascular Medicine
  • Pharmacology

Background:

  • Vascular endothelial function is impaired in patients with coronary vasospasm.
  • The differential effects of L-type calcium-channel blocker (CCB) classes on endothelial function in this population remain unclear.

Purpose of the Study:

  • To compare the effects of benidipine (dihydropyridine), diltiazem (benzothiazepine), and verapamil (phenylalkylamine) on vascular endothelial function in patients with coronary vasospasm.

Main Methods:

  • Twenty-five patients with coronary vasospasm received one of the three CCBs for 3 months.
  • Assessed were endothelium-dependent flow-mediated dilatation (FMD), endothelium-independent nitroglycerin-induced dilatation, and plasma cyclic guanosine 3',5'-monophosphate (cGMP).
  • Measurements were taken before and after the treatment period.

Main Results:

  • Patients with vasospasm exhibited lower baseline FMD compared to healthy subjects.
  • Benidipine significantly increased FMD and plasma cGMP levels.
  • Diltiazem and verapamil did not significantly alter FMD or cGMP levels; none of the drugs affected nitroglycerin-induced dilatation.

Conclusions:

  • Benidipine, a dihydropyridine CCB, improves endothelial dysfunction in coronary vasospasm patients, independent of blood pressure reduction.
  • The nitric oxide-cGMP pathway may mediate benidipine's beneficial effects.
  • Dihydropyridine CCBs might offer greater advantages for vascular endothelial function compared to non-dihydropyridine CCBs in this patient group.
Abstract

Related Concept Videos

Antihypertensive Drugs: Action of Calcium Channel Blockers01:18

Antihypertensive 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,...
Antianginal Drugs: Calcium Channel Blockers and Ranolazine01:25

Antianginal 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...
Antiarrhythmic Drugs: Class IV Agents as Calcium Channel Blockers01:20

Antiarrhythmic 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...
Antianginal Drugs: Nitrates and β-Blockers01:16

Antianginal 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...
Antihypertensive Drugs: Vasodilators01:23

Antihypertensive 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...
Heart Failure Drugs: β-Blockers01:22

Heart 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...