Related Experiment Video

Updated: Jul 14, 2026

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

Regression of nephropathy developed in diabetes by (Pro)renin receptor blockade

Hidena Takahashi1, Atsuhiro Ichihara, Yuki Kaneshiro

  • 1Department of Internal Medicine, Keio University School of Medicine, 35 Shinanomachi, Tokyo, Japan.

Journal of the American Society of Nephrology : JASN
|June 1, 2007
PubMed

Insights

Blocking the (pro)renin receptor halts diabetic nephropathy progression and reverses glomerulosclerosis in rats. This targeted approach shows promise for treating advanced kidney disease in diabetes.

Area of Science:

  • Nephrology
  • Endocrinology
  • Pharmacology

Background:

  • The (pro)renin receptor activates the tissue renin-angiotensin system, contributing to diabetic nephropathy.
  • Diabetic nephropathy is characterized by increased urinary protein excretion and glomerulosclerosis.

Purpose of the Study:

  • To investigate if (pro)renin receptor blockade can inhibit the progression of established diabetic nephropathy.
  • To evaluate the efficacy of (pro)renin receptor blockade compared to an angiotensin-converting enzyme inhibitor.

Main Methods:

  • Diabetic rats with existing nephropathy received (pro)renin receptor blocker (PRRB), ACE inhibitor (ACEi), or vehicle for 12 weeks.
  • Measurements included urinary protein excretion, glomerulosclerosis, and kidney expression of activated prorenin.

Main Results:

  • PRRB treatment prevented further increases in urinary protein and glomerulosclerosis.
  • ACEi treatment only attenuated the progression of these markers.
  • PRRB significantly suppressed activated prorenin expression in kidneys, unlike ACEi.

Conclusions:

  • (Pro)renin receptor blockade effectively inhibits diabetic nephropathy progression.
  • (Pro)renin receptor blockade may reverse existing glomerulosclerosis in diabetic rats.
  • Targeting the (pro)renin receptor offers a novel therapeutic strategy for diabetic kidney disease.

More Related Videos

Antagonistic Effect of Jiawei Shengjiang San on a Rat Model of Diabetic Nephropathy: Related to EGFR/MAPK3/1 Signaling Pathway08:15

Antagonistic Effect of Jiawei Shengjiang San on a Rat Model of Diabetic Nephropathy: Related to EGFR/MAPK3/1 Signaling Pathway

Published on: May 10, 2024

Related Concept Videos

Diabetic Nephropathy01:28

Diabetic Nephropathy

Definition Diabetic nephropathy is a chronic kidney complication that results from prolonged hyperglycemia.Prevalence It is the most common cause of chronic kidney disease (CKD) and end-stage renal disease (ESRD) worldwide, affecting up to half of individuals with diabetes.Pathophysiology • Sustained hyperglycemia triggers multiple hemodynamic and metabolic changes in the kidney. • Early in the disease, increased renal blood flow and glomerular hyperfiltration occur due to afferent arteriolar...
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,...
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
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...
Antihypertensive Drugs: Action of Diuretics01:16

Antihypertensive Drugs: Action of Diuretics

Diuretics are antihypertensive drugs used to treat hypertension resulting from sodium and water retention. Sodium, vital for fluid balance and nerve or muscle function, is regulated by the kidneys through millions of nephrons. Blood enters nephrons via afferent arterioles, which branch into capillaries called glomeruli. These filter blood plasma, allowing water and solutes, like sodium ions, to pass through capillary walls into Bowman's capsule. The filtrate then flows through various tubules...
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...