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

Serum Studies: Renal Function Tests01:24

Serum Studies: Renal Function Tests

Renal function tests are crucial for assessing kidney health, monitoring disease progression, and evaluating the kidneys' efficiency in waste elimination, fluid balance, and electrolyte regulation. These tests offer critical insights into kidney function, even though routine measurements may appear normal until there is a significant decline in the glomerular filtration rate or GFR. Typically, signs of kidney impairment only become evident when the GFR falls to about 50% of its normal level.
Nephrotic Syndrome II : Assessment and Medical Management01:26

Nephrotic Syndrome II : Assessment and Medical Management

IntroductionNephrotic syndrome is a kidney disorder marked by excessive protein loss in the urine, leading to various systemic complications. This condition often results from damage to the glomeruli—the kidney's filtering units—causing proteinuria, low blood protein levels, and fluid retention. Understanding the assessment, diagnosis, and management of nephrotic syndrome is essential for effective treatment and prevention of further kidney damage.AssessmentPatient History: Document any history...
Acute Kidney Injury IV: Diagnostic Studies and Prevention01:30

Acute Kidney Injury IV: Diagnostic Studies and Prevention

Accurate diagnosis and effective prevention are critical in managing Acute Kidney Injury (AKI), which is linked to high mortality rates ranging from 10% to 80%. Timely recognition of at-risk patients and careful monitoring can significantly reduce the likelihood of kidney damage.Diagnostic Assessments:The diagnostic process starts with a comprehensive medical history to identify prerenal, intrarenal, and postrenal causes.Prerenal causes, such as dehydration, hypotension, or blood loss, should...
Acute Kidney Injury II: Pathophysiology01:29

Acute Kidney Injury II: Pathophysiology

Acute kidney injury (AKI) causes are categorized into three primary categories based on the location of the injury: prerenal, intrarenal (or intrinsic), and postrenal causes. This classification guides clinical management and illustrates how different pathways can impair kidney function.Etiology and Pathophysiology of Acute Kidney Injury1. Prerenal causesEtiology: Prerenal Acute Kidney Injury, the most common type, occurs when reduced blood flow to the kidneys decreases filtration capacity...
Acute Kidney Injury I: Introduction01:22

Acute Kidney Injury I: Introduction

Introduction:Acute Kidney Injury (AKI) describes a swift decrease in kidney function occurring over hours to days, characterized by the kidneys' failure to remove waste products from the bloodstream. This leads to dangerous complications like metabolic acidosis, fluid overload, and electrolyte imbalances, such as hyperkalemia, which can cause life-threatening arrhythmias. AKI is common in both hospital and outpatient settings, often triggered by dehydration, sepsis, or exposure to nephrotoxic...
Antihypertensive Drugs: Direct Renin Inhibitors01:25

Antihypertensive Drugs: Direct Renin Inhibitors

The renin-angiotensin-aldosterone system (RAAS) is an intricate physiological pathway involving numerous enzymes and hormones, including renin, angiotensin-converting enzyme (ACE), angiotensin I and II, and aldosterone. Imbalances within this system increase the production of angiotensin II and aldosterone. Increased angiotensin II levels promote vasoconstriction and blood pressure elevation. Concurrently, higher aldosterone levels stimulate sodium and water reabsorption in the kidneys,...

You might also read

Related Articles

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

Sort by
Same author

Nitric oxide, prostanoids, cyclooxygenase, and angiogenesis in colon and breast cancer.

Clinical cancer research : an official journal of the American Association for Cancer Research·2001
Same author

Effect of cyclooxygenase-2 inhibitor (celecoxib) on the infarcted heart in situ.

Pharmacology·2001
Same author

Myocardial ischemia and infarction: growth of ideas.

Cardiovascular research·2001
Same author

Some aspects of biochemistry of myocardial infarction.

Cellular and molecular life sciences : CMLS·2001
Same author

Nitric oxide donors.

Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.)·2000
Same author

The effect of aspirin and two nitric oxide donors on the infarcted heart in situ.

Life sciences·2000
Same journal

Intravesical mesothelin-based CAR T cells targeting MUC16 effectively control bladder cancer in preclinical models.

The Journal of experimental medicine·2026
Same journal

Flawed translation triggers oncogenic B-T cell communication.

The Journal of experimental medicine·2026
Same journal

Mechanobiology of inflammation: Pulling the strings of innate immunity.

The Journal of experimental medicine·2026
Same journal

Bile acid retention in efferocytic macrophages shapes their inflammatory status during cholangitis.

The Journal of experimental medicine·2026
Same journal

Endothelial cells notch monocytes toward an alveolar macrophage fate.

The Journal of experimental medicine·2026
Same journal

UBE2F impedes CD8 T cell memory.

The Journal of experimental medicine·2026
See all related articles

Related Experiment Video

Updated: Jun 19, 2026

5/6th Nephrectomy in Combination with High Salt Diet and Nitric Oxide Synthase Inhibition to Induce Chronic Kidney Disease in the Lewis Rat
08:50

5/6th Nephrectomy in Combination with High Salt Diet and Nitric Oxide Synthase Inhibition to Induce Chronic Kidney Disease in the Lewis Rat

Published on: July 3, 2013

RENAL HYPERTENSION PRODUCED BY AN AMINO ACID.

R J Bing1, M B Zucker

  • 1Department of Physiology, College of Physicians and Surgeons, Columbia University, New York.

The Journal of Experimental Medicine
|October 30, 2009
PubMed
Summary
This summary is machine-generated.

Injecting dopa (l-dihydroxyphenylalanine) into ischemic cat kidneys causes acute renal hypertension. This rise in blood pressure results from dopa converting to hydroxytyramine, a pressor amine, a process not seen in healthy kidneys.

More Related Videos

A Large Animal Model for Acute Kidney Injury by Temporary Bilateral Renal Artery Occlusion
09:02

A Large Animal Model for Acute Kidney Injury by Temporary Bilateral Renal Artery Occlusion

Published on: February 2, 2021

Related Experiment Videos

Last Updated: Jun 19, 2026

5/6th Nephrectomy in Combination with High Salt Diet and Nitric Oxide Synthase Inhibition to Induce Chronic Kidney Disease in the Lewis Rat
08:50

5/6th Nephrectomy in Combination with High Salt Diet and Nitric Oxide Synthase Inhibition to Induce Chronic Kidney Disease in the Lewis Rat

Published on: July 3, 2013

A Large Animal Model for Acute Kidney Injury by Temporary Bilateral Renal Artery Occlusion
09:02

A Large Animal Model for Acute Kidney Injury by Temporary Bilateral Renal Artery Occlusion

Published on: February 2, 2021

Area of Science:

  • Nephrology
  • Cardiovascular Physiology
  • Biochemistry

Background:

  • Acute renal hypertension is a critical condition affecting kidney function.
  • Understanding the mechanisms behind renal hypertension is crucial for developing effective treatments.
  • The role of specific amino acids and their metabolites in blood pressure regulation requires further investigation.

Purpose of the Study:

  • To investigate the effect of dopa (l-dihydroxyphenylalanine) injection on blood pressure in ischemic kidneys.
  • To determine the biochemical pathway responsible for dopa-induced hypertension in renal ischemia.
  • To compare the metabolic fate of dopa in ischemic versus non-ischemic kidneys.

Main Methods:

  • Cats underwent partial or complete kidney ischemia.
  • Dopa (l-dihydroxyphenylalanine) was injected into the ischemic kidneys.
  • Blood pressure was monitored following dopa administration.
  • The conversion of dopa to hydroxytyramine was assessed.

Main Results:

  • Dopa injection into ischemic kidneys produced acute renal hypertension.
  • The pressor effect was attributed to the conversion of dopa into hydroxytyramine.
  • Kidneys with normal blood flow did not transform dopa into a pressor substance.

Conclusions:

  • Dopa can induce acute renal hypertension in ischemic kidneys through its conversion to hydroxytyramine.
  • Kidney ischemia is a prerequisite for the conversion of dopa into a pressor agent.
  • This study elucidates a novel mechanism contributing to renal hypertension.