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

Sympathetic Activation01:16

Sympathetic Activation

The sympathetic division can influence tissues and organs by releasing norepinephrine at peripheral synapses and distributing epinephrine and norepinephrine through the bloodstream. In times of crisis or stress, sympathetic activation occurs, which is regulated by sympathetic centers in the hypothalamus. As a result, sympathetic activation prepares the body for physical exertion, rapid ATP production, and heightened alertness, allowing individuals to respond effectively to challenging or...
Heart Failure II: Pathophysiology01:29

Heart Failure II: Pathophysiology

Systolic Heart Failure and Compensatory MechanismsSystolic heart failure (also termed HFrEF, Heart Failure with Reduced Ejection Fraction) is the most prevalent type of heart filure. It results in a decreased volume of blood being pumped from the ventricle. The aortic arch and carotid sinuses have baroreceptors that detect reduced blood pressure, triggering the sympathetic nervous system (SNS) to release epinephrine and norepinephrine. Initially, this response aims to boost heart rate and...
Sympathetic Signaling01:31

Sympathetic Signaling

Sympathetic signaling, a vital part of the autonomic nervous system, plays a crucial role in mobilizing the body's resources in response to stress or emergencies. It involves the transmission of nerve impulses from sympathetic preganglionic fibers to postganglionic fibers. This results in the release of specific neurotransmitters and activation of adrenergic receptors.
Sympathetic preganglionic fibers release the neurotransmitter acetylcholine (ACh) onto the ganglionic neurons in the...
Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists01:18

Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists

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 (ECE). Of...
Regulation of Food Intake01:30

Regulation of Food Intake

Short-term regulation of food intake primarily involves neural signals from the gastrointestinal (GI) tract, blood nutrient levels, and GI tract hormones. Communication between the gut and brain via vagal nerve fibers plays a significant role in evaluating the contents of the gut. Clinical studies have shown that protein ingestion produces a more prolonged response in these nerve fibers compared to an equivalent amount of glucose. Additionally, the activation of stretch receptors caused by GI...
Disorders of the Autonomic Nervous System01:18

Disorders of the Autonomic Nervous System

The autonomic nervous system (ANS) is an intricate network of nerves that controls functions such as the regulation of heart rate, digestion, and blood pressure regulation. When this system malfunctions, it can lead to various disorders that affect multiple bodily functions. One common feature of many autonomic disorders is the involvement of smooth blood vessels, which play a crucial role in regulating blood flow throughout the body.
Raynaud's disease, also known as Raynaud's phenomenon, is a...

You might also read

Related Articles

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

Sort by
Same author

Sickle hemoglobin promotes venous thrombosis through procoagulant activity and is targetable by hemoglobinase therapy.

Journal of thrombosis and haemostasis : JTH·2026
Same author

The first in-human study to evaluate the antiplatelet properties of the clopidogrel conjugate DT-678 in acute coronary syndrome patients and healthy volunteers.

British journal of pharmacology·2024
Same author

Inhibition of sodium-glucose cotransporter-2 improves anaemia in mice and humans with sickle cell disease, and reduces infarct size in a murine stroke model.

Journal of cellular and molecular medicine·2024
Same author

Resolution of Sickle Cell Crisis Following Administration of Amiodarone.

European journal of case reports in internal medicine·2023
Same author

Beta1-receptor blockade attenuates atherosclerosis progression following traumatic brain injury in apolipoprotein E deficient mice.

PloS one·2023
Same author

Amiodarone improves anemia in a murine model of sickle cell disease and is associated with increased erythrocyte bis(monoacylglycerol) phosphate.

Scientific reports·2022

Related Experiment Video

Updated: May 7, 2026

Experimental Approach to Examine Leptin Signaling in the Carotid Bodies and its Effects on Control of Breathing
05:45

Experimental Approach to Examine Leptin Signaling in the Carotid Bodies and its Effects on Control of Breathing

Published on: October 25, 2019

Leptin-induced endothelial dysfunction is mediated by sympathetic nervous system activity.

Jintao Wang1, Hui Wang, Wei Luo

  • 1Department of Internal Medicine, Cardiovascular Research Center, University of Michigan, Ann Arbor, MI.

Journal of the American Heart Association
|September 18, 2013
PubMed
Summary

Leptin, elevated in obesity, impairs blood vessel function by activating the sympathetic nervous system and increasing oxidative stress. This contributes to hypertension and vascular stiffness.

Keywords:
ganglionectomyhypertensionnervous systemobesitysuperoxide

More Related Videos

Screening Assays to Characterize Novel Endothelial Regulators Involved in the Inflammatory Response
12:50

Screening Assays to Characterize Novel Endothelial Regulators Involved in the Inflammatory Response

Published on: September 15, 2017

Quantifying Acute Changes in Renal Sympathetic Nerve Activity in Response to Central Nervous System Manipulations in Anesthetized Rats
06:30

Quantifying Acute Changes in Renal Sympathetic Nerve Activity in Response to Central Nervous System Manipulations in Anesthetized Rats

Published on: September 11, 2018

Related Experiment Videos

Last Updated: May 7, 2026

Experimental Approach to Examine Leptin Signaling in the Carotid Bodies and its Effects on Control of Breathing
05:45

Experimental Approach to Examine Leptin Signaling in the Carotid Bodies and its Effects on Control of Breathing

Published on: October 25, 2019

Screening Assays to Characterize Novel Endothelial Regulators Involved in the Inflammatory Response
12:50

Screening Assays to Characterize Novel Endothelial Regulators Involved in the Inflammatory Response

Published on: September 15, 2017

Quantifying Acute Changes in Renal Sympathetic Nerve Activity in Response to Central Nervous System Manipulations in Anesthetized Rats
06:30

Quantifying Acute Changes in Renal Sympathetic Nerve Activity in Response to Central Nervous System Manipulations in Anesthetized Rats

Published on: September 11, 2018

Area of Science:

  • Cardiovascular Physiology
  • Endocrinology
  • Vascular Biology

Background:

  • Leptin, an adipocyte hormone, is elevated in obesity and linked to increased vascular risk.
  • The precise mechanisms by which leptin influences vascular disease remain unclear.
  • Leptin has been observed to increase sympathetic nervous system activity.

Purpose of the Study:

  • To investigate the impact of leptin on endothelial function.
  • To determine the role of the local sympathetic nervous system in mediating leptin's vascular effects.

Main Methods:

  • Administration of recombinant leptin to C57BL6/J mice.
  • Mesenteric arteriole myography to assess vasorelaxation.
  • Evaluation of blood pressure responses to angiotensin II.
  • Sympathetic denervation of mesenteric vasculature and use of superoxide scavenger TEMPOL.

Main Results:

  • Leptin treatment impaired endothelium-dependent vasorelaxation.
  • Leptin augmented the blood pressure response to angiotensin II.
  • Sympathetic denervation and TEMPOL neutralized leptin's effects on vascular function and blood pressure.

Conclusions:

  • Leptin induces endothelial dysfunction and potentiates angiotensin II-mediated hypertension.
  • These effects are mediated by sympathetic nervous system activation and superoxide production.
  • Leptin's actions may contribute to obesity-associated vascular stiffness and hypertension.