Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists01:18

Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists

464
Endothelins (ETs) are potent vasoactive peptides critical in the human body's various physiological and pathological processes. One of the most promising therapeutic strategies for treating pulmonary arterial hypertension (PAH) involves counteracting the effects of these endothelins using a class of drugs known as endothelin receptor antagonists.
ETs are synthesized through a complex sequence of enzymatic steps, primarily involving an enzyme referred to as endothelin-converting enzyme...
464
Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists01:23

Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists

495
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...
495
Internal Receptors01:31

Internal Receptors

74.6K
Many cellular signals are hydrophilic and therefore cannot pass through the plasma membrane. However, small or hydrophobic signaling molecules can cross the hydrophobic core of the plasma membrane and bind to internal, or intracellular, receptors that reside within the cell. Many mammalian steroid hormones use this mechanism of cell signaling, as does nitric oxide (NO) gas.
74.6K
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

518
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...
518
Hypertension I: Introduction01:28

Hypertension I: Introduction

848
Hypertension is a widespread, long-term medical condition where blood pressure in the arteries remains elevated. It is characterized by systolic blood pressure readings of 130 mm Hg or above or diastolic blood pressure (DBP) readings of 80 mm Hg or higher. Unmanaged hypertension poses significant health risks, making the distinction between primary (or essential) hypertension and secondary hypertension crucial, as their management and implications vary.Primary HypertensionPrimary hypertension,...
848
Hypertension II: Pathophysiology01:29

Hypertension II: Pathophysiology

915
Hypertension is a chronic condition in which the blood's force against artery walls is excessively high, posing risks such as heart disease. The condition's underlying mechanisms involve complex interactions among the cardiovascular, kidney, and autonomic nervous systems.Renin-Angiotensin-Aldosterone System (RAAS): This system significantly influences blood pressure regulation. When blood pressure decreases, the kidneys secrete renin. This enzyme transforms angiotensinogen, a plasma protein,...
915

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

IMD-0354 optimization generates potent colistin adjuvants with in vivo activity and reduced eukaryotic toxicity.

European journal of medicinal chemistry·2026
Same author

Temperature reorganises developmental time during thyroid hormone-driven fish metamorphosis.

Developmental biology·2026
Same author

Osborne's ligament: Anatomical study with application to better understanding ulnar nerve compression at the elbow.

Neurosurgical review·2026
Same author

A Survey of Home Dialysis Competency, Exposure, and Barriers Among Nephrology Fellows in the United States.

American journal of kidney diseases : the official journal of the National Kidney Foundation·2026
Same author

Sports Nephrology: From Bench to Bedside.

Clinical journal of the American Society of Nephrology : CJASN·2026
Same author

Mice humanized by syntenic replacement with full-length NLRP3 disease-associated variants model the clinical cryopyrinopathy continuum.

JCI insight·2026

Related Experiment Video

Updated: Jan 29, 2026

The Role of Indocyanine Green Fluorescence in Complex Laparoscopic Cholecystectomy Navigation
03:27

The Role of Indocyanine Green Fluorescence in Complex Laparoscopic Cholecystectomy Navigation

Published on: January 31, 2025

1.3K

Complex Role for E-Prostanoid 4 Receptors in Hypertension.

Marcela Herrera1, Ting Yang1, Matthew A Sparks1,2

  • 11 Division of Nephrology Department of Medicine Duke University Durham NC.

Journal of the American Heart Association
|February 16, 2019
PubMed
Summary

The EP 4 receptor (EP 4R) plays a complex role in blood pressure regulation. Its absence increases blood pressure and hypertension, but its specific functions in vascular smooth muscle are paradoxical.

Keywords:
E‐prostanoid 4 receptorangiotensin IIblood pressurehypertensionprostaglandin E2reninvascular smooth muscle cells

More Related Videos

Biochemical Reconstitution of Steroid Receptor•Hsp90 Protein Complexes and Reactivation of Ligand Binding
11:07

Biochemical Reconstitution of Steroid Receptor•Hsp90 Protein Complexes and Reactivation of Ligand Binding

Published on: September 21, 2011

16.9K
Improved Renal Denervation Mitigated Hypertension Induced by Angiotensin II Infusion
08:35

Improved Renal Denervation Mitigated Hypertension Induced by Angiotensin II Infusion

Published on: May 26, 2022

4.1K

Related Experiment Videos

Last Updated: Jan 29, 2026

The Role of Indocyanine Green Fluorescence in Complex Laparoscopic Cholecystectomy Navigation
03:27

The Role of Indocyanine Green Fluorescence in Complex Laparoscopic Cholecystectomy Navigation

Published on: January 31, 2025

1.3K
Biochemical Reconstitution of Steroid Receptor•Hsp90 Protein Complexes and Reactivation of Ligand Binding
11:07

Biochemical Reconstitution of Steroid Receptor•Hsp90 Protein Complexes and Reactivation of Ligand Binding

Published on: September 21, 2011

16.9K
Improved Renal Denervation Mitigated Hypertension Induced by Angiotensin II Infusion
08:35

Improved Renal Denervation Mitigated Hypertension Induced by Angiotensin II Infusion

Published on: May 26, 2022

4.1K

Area of Science:

  • Cardiovascular Physiology
  • Molecular Pharmacology
  • Hypertension Research

Background:

  • Prostaglandin E2 (PGE2) influences blood pressure via four E-prostanoid (EP) receptors.
  • EP 4 receptor (EP 4R) mediates PGE2-induced vasodilation, but its role in hypertension is unclear.

Purpose of the Study:

  • Investigate the role of EP 4R in blood pressure regulation and hypertension pathogenesis.
  • Determine the specific contribution of EP 4R in vascular smooth muscle to these effects.

Main Methods:

  • Utilized mice with temporal and cell-specific deletion of EP 4R.
  • Assessed blood pressure responses to PGE2 infusion, high salt diet, and angiotensin II.
  • Compared generalized EP 4R deficiency with EP 4R loss restricted to vascular smooth muscle.

Main Results:

  • Generalized EP 4R deficiency increased resting blood pressure and exacerbated hypertension.
  • EP 4R is crucial for acute PGE2-mediated vasodilation and limiting angiotensin II-induced hypertension.
  • EP 4R deletion in vascular smooth muscle alone paradoxically lowered resting blood pressure but did not affect angiotensin II-induced hypertension.

Conclusions:

  • EP 4R has a multifaceted role in blood pressure homeostasis and hypertension.
  • EP 4R's functions extend beyond vascular smooth muscle, involving other tissues.
  • Further research is needed to elucidate the complex mechanisms of EP 4R in cardiovascular health.