Related Experiment Video

Updated: Apr 27, 2026

A Modified Two Kidney One Clip Mouse Model of Renin Regulation in Renal Artery Stenosis
08:21

A Modified Two Kidney One Clip Mouse Model of Renin Regulation in Renal Artery Stenosis

Published on: October 26, 2020

4.9K

Large blood pressure variability aggravates arteriolosclerosis and cortical sclerotic changes in the kidney in

Yuji Aoki1, Hisashi Kai, Hidemi Kajimoto

  • 1Department of Internal Medicine, Division of Cardio-Vascular Medicine, Kurume University School of Medicine.

Circulation Journal : Official Journal of the Japanese Circulation Society
|July 1, 2014
PubMed

Insights

Large blood pressure variability (BPV) causes kidney damage in hypertensive rats by affecting blood vessels. Candesartan, an angiotensin II receptor blocker, protected against this renal damage, suggesting its potential for patients with hypertension and high BPV.

Area of Science:

  • Cardiovascular Research
  • Nephrology
  • Pharmacology

Background:

  • Increased short-term blood pressure variability (BPV) worsens cardiac remodeling in spontaneously hypertensive rats (SHRs) via the cardiac angiotensin II (AngII) system.
  • The impact of large BPV on renal damage in SHRs was previously unknown.
  • This study investigated kidney histology and the protective effects of candesartan, an AngII type 1 receptor blocker (ARB), in SHRs with large BPV.

Purpose of the Study:

  • To investigate the renal damage induced by large blood pressure variability (BPV) in spontaneously hypertensive rats (SHRs).
  • To determine if candesartan, an angiotensin II receptor blocker (ARB), can prevent renal damage in SHRs with large BPV.

Main Methods:

  • Created a model of hypertension and large BPV in SHRs by performing bilateral sinoaortic denervation (SAD).
  • Assessed histological changes in the kidney seven weeks post-SAD.
  • Administered chronic treatment with a subdepressor dose of candesartan.

Main Results:

  • SAD increased BPV without altering mean blood pressure.
  • SAD induced focal sclerotic lesions, interstitial fibrosis, and ischemic changes in the renal cortex.
  • Arteriolosclerotic changes with vascular smooth muscle cell proliferation and matrix deposition led to pre-glomerular arteriole narrowing and occlusion.
  • Candesartan treatment prevented arteriolosclerosis and cortical lesions in SAD-SHRs without affecting BPV.

Conclusions:

  • Large BPV exacerbates pre-glomerular arteriolosclerosis, leading to cortical sclerotic changes in SHRs through a local AngII-mediated mechanism.
  • Angiotensin II receptor blockers (ARBs) may offer renal protection in hypertensive patients with increased BPV.
Abstract

More Related Videos

Simultaneous Electrocardiography Recording and Invasive Blood Pressure Measurement in Rats07:35

Simultaneous Electrocardiography Recording and Invasive Blood Pressure Measurement in Rats

Published on: January 31, 2019

15.4K
Assessment of Vascular Function in Patients With Chronic Kidney Disease08:50

Assessment of Vascular Function in Patients With Chronic Kidney Disease

Published on: June 16, 2014

15.4K

Related Concept Videos

Hypertension and Regulation of Blood Pressure01:18

Hypertension and Regulation of Blood Pressure

Hypertension, the most common cardiovascular disease, is diagnosed through repeated measurements of elevated blood pressure. Its risks, including damage to the kidney, heart, and brain, are directly proportional to blood pressure levels. Starting from 115/75 mm Hg, the risk of cardiovascular disease doubles with each increment of 20/10 mm Hg. The diagnosis relies on blood pressure measurements, not on patient symptoms, as hypertension is often asymptomatic until end-organ damage is imminent or...
3.8K
Hypertension II: Pathophysiology01:29

Hypertension II: Pathophysiology

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,...
1.7K
Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors01:30

Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors

Angiotensin-converting enzyme (ACE), a vital component of the renin-angiotensin-aldosterone system, is abundant in lung endothelial cells. ACE converts the inactive decapeptide, angiotensin I, into the active octapeptide, angiotensin II. This potent vasoconstrictor narrows blood vessels, increasing resistance to blood flow and elevating blood pressure. Angiotensin II also stimulates aldosterone production, encouraging kidney cells to reabsorb more sodium and water from urine, thereby increasing...
2.7K
Antihypertensive Drugs: Angiotensin II Receptor Blockers01:30

Antihypertensive Drugs: Angiotensin II Receptor Blockers

In the renin-angiotensin-aldosterone system, a hormone called angiotensin II plays a crucial role. It binds to the AT1 receptors in vascular smooth muscles coupled with Gq proteins. The activation of these receptors activates an enzyme called phospholipase C, which releases two molecules: inositol trisphosphate and diacylglycerol. These molecules cause a chain reaction that leads to the phosphorylation of myosin light chains and promotes interaction between actin and myosin, leading to smooth...
2.9K
Hypertension III: Clinical Manifestations and Diagnostic Studies01:30

Hypertension III: Clinical Manifestations and Diagnostic Studies

Hypertension is asymptomatic and also referred to as the "silent killer" until it progresses to a severe stage or causes target organ disease. Patients may experience symptoms stemming from the strain on blood vessels and tissues in various organs or the heart's increased workload.Physical exams might show no abnormalities other than high blood pressure. Signs of vascular damage, when present, correspond to the organs supplied by the affected vessels, leading to target organ damage. For...
851
Antihypertensive Drugs: Action of β1 Blockers01:17

Antihypertensive Drugs: Action of β1 Blockers

β1-receptors are primarily located in the heart and kidneys. In cardiac myocytes, these receptors interact with neurotransmitters released by the sympathetic nervous system during heightened activity or danger. As a result, β1-receptors get activated, initiating a series of biochemical processes. Excessive activation of beta receptors due to chronic stress can abnormally increase heart rate and contractility, resulting in high blood pressure or hypertension. To counteract this,...
2.2K