Related Experiment Video

Updated: Aug 16, 2026

Intracoronary Acetylcholine Provocation Testing for Assessment of Coronary Vasomotor Disorders
06:39

Intracoronary Acetylcholine Provocation Testing for Assessment of Coronary Vasomotor Disorders

Published on: August 18, 2016

Cyclic adenosine monophosphate antagonism of prostaglandin induced vasospasm

E W Peterson, R Leblanc, F Lebel

    Surgical Neurology
    |December 1, 1975
    PubMed

    More Related Videos

    Testing Acetylcholine Followed by Adenosine for Invasive Diagnosis of Coronary Vasomotor Disorders05:58

    Testing Acetylcholine Followed by Adenosine for Invasive Diagnosis of Coronary Vasomotor Disorders

    Published on: February 3, 2021

    Isolation of Intrapulmonary Artery and Smooth Muscle Cells to Investigate Vascular Responses07:56

    Isolation of Intrapulmonary Artery and Smooth Muscle Cells to Investigate Vascular Responses

    Published on: June 8, 2022

    Related Concept Videos

    GPCRs Regulate Adenylyl Cylase Activity01:09

    GPCRs Regulate Adenylyl Cylase Activity

    Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of cells.
    Two...
    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...
    Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors01:20

    Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors

    Antiplatelet drugs emerge as frontline defenders against the insidious threat of thromboembolic diseases, where abnormal clots obstruct vital blood vessels. These drugs stand as bulwarks, inhibiting platelet aggregation and clot formation, thereby mitigating the risk of life-threatening conditions like myocardial infarction, coronary artery disease, and thrombotic strokes.
    Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
    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...
    Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists01:23

    Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists

    Prostacyclin receptor agonists are a class of therapeutic agents integral to managing pulmonary arterial hypertension (PAH). These drugs operate by mimicking the action of prostaglandin I2, or PGI2, a naturally occurring compound in the body.
    These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...
    Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents01:20

    Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents

    The gastric mucosa produces prostaglandins E2 (PGE2) and prostacyclin (PGI2), crucial in maintaining gastric health. They exert cytoprotective effects, including increasing bicarbonate secretion, releasing protective mucin, reducing gastric acid output, and preventing harmful vasoconstriction. These effects are mediated through various receptors, such as EP1, EP2, EP3, and EP4.
    Non-steroidal anti-inflammatory drugs (NSAIDs) can induce peptic ulcers by inhibiting cyclooxygenase, decreasing...