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Related Concept Videos

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.
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Lipid-Lowering Drugs: Statins and Miscellaneous Agents01:20

Lipid-Lowering Drugs: Statins and Miscellaneous Agents

Hyperlipidemia, a medical condition often referred to as high cholesterol, is characterized by abnormally elevated levels of lipids in the bloodstream. When present in excess, these lipids, specifically cholesterol and triglycerides, can lead to serious health complications, often involving cardiovascular diseases. Illnesses like atherosclerosis, heart attacks, and pancreatitis have all been linked to untreated hyperlipidemia. This means controlling and regulating cholesterol and triglyceride...
Antianginal Drugs: Calcium Channel Blockers and Ranolazine01:25

Antianginal Drugs: Calcium Channel Blockers and Ranolazine

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Treatment for Pulmonary Arterial Hypertension: Receptor Tyrosine Kinase Inhibitors and Calcium Channel Blockers01:26

Treatment for Pulmonary Arterial Hypertension: Receptor Tyrosine Kinase Inhibitors and Calcium Channel Blockers

Receptor tyrosine kinase inhibitors (TKIs) and calcium channel blockers (CCBs) are two critical categories of drugs employed in the treatment of pulmonary artery hypertension (PAH). PAH is a disease that causes high blood pressure in the pulmonary arteries, resulting in chest pain, fatigue, and shortness of breath.
TKIs, such as imatinib (Gleevec), are particularly effective in tackling the growth and mitogenic factors that become upregulated in PAH patients. These factors contribute to the...
Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists01:18

Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists

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Antihypertensive Drugs: Vasodilators01:23

Antihypertensive Drugs: Vasodilators

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Related Experiment Video

Updated: Jun 12, 2026

In vivo Near Infrared Fluorescence (NIRF) Intravascular Molecular Imaging of Inflammatory Plaque, a Multimodal Approach to Imaging of Atherosclerosis
09:43

In vivo Near Infrared Fluorescence (NIRF) Intravascular Molecular Imaging of Inflammatory Plaque, a Multimodal Approach to Imaging of Atherosclerosis

Published on: August 4, 2011

Niacin and laropiprant.

S Sanyal1, J T Kuvin, R H Karas

  • 1Division of Cardiology, Department of Medicine, Preventive Cardiology Center, Tufts Medical Center, Boston, MA 02111, USA. rkaras@tuftsmedicalcenter.org

Drugs of Today (Barcelona, Spain : 1998)
|June 24, 2010
PubMed
Summary
This summary is machine-generated.

Niacin effectively raises HDL cholesterol but causes flushing. Combining niacin with laropiprant, a prostaglandin receptor antagonist, reduces flushing and improves patient compliance without impacting lipid benefits.

Related Experiment Videos

Last Updated: Jun 12, 2026

In vivo Near Infrared Fluorescence (NIRF) Intravascular Molecular Imaging of Inflammatory Plaque, a Multimodal Approach to Imaging of Atherosclerosis
09:43

In vivo Near Infrared Fluorescence (NIRF) Intravascular Molecular Imaging of Inflammatory Plaque, a Multimodal Approach to Imaging of Atherosclerosis

Published on: August 4, 2011

Area of Science:

  • Cardiovascular Medicine
  • Pharmacology

Background:

  • Nicotinic acid (niacin) is a long-standing treatment for dyslipidemia.
  • Niacin effectively raises high-density lipoprotein cholesterol (HDL-C) and lowers low-density lipoprotein cholesterol (LDL-C).
  • Niacin-induced flushing is a significant side effect limiting patient adherence.

Purpose of the Study:

  • To review the importance of raising HDL-C with niacin.
  • To describe the pharmacology of niacin.
  • To examine the benefits of combining niacin with laropiprant.

Main Methods:

  • Review of existing clinical data and pharmacological studies.
  • Elucidation of the molecular mechanism of niacin-induced flushing.
  • Evaluation of laropiprant as a selective prostaoid DP(1) receptor antagonist.

Main Results:

  • Niacin stimulates prostaglandin production, mediating flushing.
  • Laropiprant effectively reduces the incidence and intensity of niacin-induced flushing.
  • Laropiprant does not interfere with the beneficial lipid-modifying effects of niacin.

Conclusions:

  • Combining niacin with laropiprant improves niacin's tolerability.
  • Laropiprant enhances patient compliance with niacin therapy.
  • The combination therapy offers a promising approach to managing dyslipidemia.