Related Experiment Video
Updated: Jul 31, 2026
05:58
Testing Acetylcholine Followed by Adenosine for Invasive Diagnosis of Coronary Vasomotor Disorders
Published on: February 3, 2021
Haemodynamic differences between cromakalim and pinacidil: comparison with nifedipine
1Beecham Pharmaceuticals Research Division, Medicinal Research Centre, Harlow, Essex, U.K.
European Journal of Pharmacology
|November 14, 1989
Summary
Cromakalim, pinacidil, and nifedipine affect blood pressure differently in cats. Cromakalim uniquely increases renal blood flow, unlike the other two drugs, indicating distinct cardiovascular effects.
Area of Science:
- Pharmacology
- Cardiovascular Physiology
Background:
- Potassium channel openers and calcium channel blockers are used to manage hypertension.
- Understanding their distinct hemodynamic profiles is crucial for therapeutic application.
Purpose of the Study:
- To compare the cardiovascular and renal effects of cromakalim, pinacidil, and nifedipine in conscious cats.
- To investigate whether increased renal blood flow is a general effect of K+ channel activation or Ca2+ channel blockade.
Main Methods:
- Conscious normotensive cats were administered varying oral doses of cromakalim, pinacidil, and nifedipine.
- Mean arterial pressure (MAP), heart rate (HR), mean renal blood flow (MRBF), and plasma renin activity (PRA) were measured.
Main Results:
- All drugs dose-dependently reduced MAP; cromakalim was most potent.
- Cromakalim produced smaller increases in HR and PRA compared to nifedipine and pinacidil for similar MAP reduction.
- Cromakalim dose-dependently increased MRBF, while nifedipine and pinacidil did not.
Conclusions:
- Significant hemodynamic differences exist between cromakalim, nifedipine, and pinacidil.
- Increased MRBF is not a universal outcome of K+ channel activation or Ca2+ channel blockade.
Related Concept Videos
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...
01:18Antihypertensive 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,...
01:23Antihypertensive 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...
01:24Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers
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 indirectly block calcium...
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...