Related Experiment Video

Updated: Oct 10, 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 left ventricular hypertrophy by AT1 receptor blockade in renal transplant recipients

A U Klingbeil1, H J Müller, C Delles

  • 1Department of Medicine IV and Nephrology, University of Erlangen-Nürnberg, Germany.

American Journal of Hypertension
|December 29, 2000
PubMed

Insights

Losartan effectively reduces blood pressure and left ventricular hypertrophy in kidney transplant recipients. This AT1 receptor antagonist is safe for renal function and immunosuppression, though it may slightly lower hemoglobin levels.

Area of Science:

  • Cardiology
  • Nephrology
  • Pharmacology

Background:

  • Left ventricular hypertrophy (LVH) is prevalent in renal transplant recipients.
  • AT1 receptor antagonists are effective in managing hypertension and LVH.

Purpose of the Study:

  • To evaluate the cardiovascular effects and safety of losartan in hypertensive renal transplant recipients.
  • To assess losartan's impact on blood pressure, cardiac structure, and renal function post-transplant.

Main Methods:

  • 20 hypertensive renal transplant recipients received losartan (50 mg daily) for 6 months.
  • Evaluated 24-h ambulatory blood pressure, echocardiography, duplex sonography, and laboratory parameters.
  • Monitored renal function, blood counts, immunosuppressant levels (cyclosporine A, FK 506), and erythropoietin.

Main Results:

  • Significant reductions in systolic (7.5 mmHg) and diastolic (4.5 mmHg) blood pressure observed.
  • Marked decrease in posterior wall thickness, septal thickness, and left ventricular mass index (18.1 g/m2).
  • No significant changes in ejection fraction or diastolic filling parameters; renal function and cyclosporine A levels remained stable. Hemoglobin and hematocrit showed a slight decrease.

Conclusions:

  • Losartan effectively reduces left ventricular hypertrophy and controls blood pressure in renal transplant recipients.
  • The drug is safe concerning renal function and immunosuppression.
  • A slight decrease in hemoglobin levels was noted, warranting monitoring.

More Related Videos

Technique of Minimally Invasive Transverse Aortic Constriction in Mice for Induction of Left Ventricular Hypertrophy08:34

Technique of Minimally Invasive Transverse Aortic Constriction in Mice for Induction of Left Ventricular Hypertrophy

Published on: September 25, 2017

A Model of Cardiac Remodeling Through Constriction of the Abdominal Aorta in Rats07:31

A Model of Cardiac Remodeling Through Constriction of the Abdominal Aorta in Rats

Published on: December 2, 2016

Related Concept Videos

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...
Heart Failure Drugs: Diuretics01:22

Heart Failure Drugs: Diuretics

Heart failure and kidney perfusion are interconnected in a complex way. Reduced renal perfusion and venous congestion are two significant factors that contribute to renal dysfunction in heart failure. The kidneys, primarily responsible for fluid balance in the body, are adversely affected due to compromised cardiac output and increased venous pressure. In response to reduced renal perfusion, the kidneys activate neurohumoral mechanisms to restore balance. However, these mechanisms can be...
Aortic Regurgitation III: Medical Management01:25

Aortic Regurgitation III: Medical Management

Aortic regurgitation (AR) is when the aortic valve does not close or seal properly, leading to backward blood circulation from the aorta into the left ventricle during diastole. Common causes of AR include rheumatic heart disease, congenital valve defects, and aortic root dilation. Managing AR requires a multifaceted approach to alleviate symptoms, preserve left ventricular function, and address the underlying cause of the regurgitation. Patients with symptomatic AR or significant left...
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...
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, β1-blockers...