Abnormal polyamine metabolism in hypertensive cardiac hypertrophy

M Shimizu1, I Masuda, K Aihara

  • 1Third Department of Internal Medicine, Jikei University School of Medicine, Tokyo, Japan.

Insights

This study investigated hypertensive cardiac hypertrophy in rats using polyamine levels. Captopril suppressed cardiac hypertrophy, while diltiazem did not, indicating its inhibitory effect.

Area of Science:

  • Cardiology
  • Pharmacology
  • Biochemistry

Background:

  • Hypertensive cardiac hypertrophy is a significant clinical concern.
  • Polyamines, such as spermidine, play a role in cellular growth and hypertrophy.
  • Understanding the impact of antihypertensive agents on cardiac hypertrophy is crucial.

Purpose of the Study:

  • To assess myocardial hypertrophic activity in spontaneously hypertensive rats (SHR) and Wistar Kyoto (WKY) rats.
  • To evaluate the effects of diltiazem, hydralazine, and captopril on hypertensive cardiac hypertrophy.
  • To determine if myocardial polyamine concentrations can serve as indicators of hypertrophic activity.

Main Methods:

  • Analysis of myocardial polyamine concentrations in SHR and WKY rats.
  • Administration of diltiazem, hydralazine, and captopril to SHR rats for 5 weeks.
  • Measurement of blood pressure, heart weight, and spermidine concentration.

Main Results:

  • SHR rats exhibited elevated blood pressure, enlarged hearts, and higher myocardial spermidine compared to WKY rats.
  • Diltiazem treatment lowered blood pressure but did not prevent increases in heart weight or spermidine.
  • Hydralazine suppressed blood pressure and spermidine increases but not heart weight increase.
  • Captopril suppressed increases in blood pressure, heart weight, and spermidine concentration.

Conclusions:

  • Spermidine concentration is a sensitive indicator of cardiac hypertrophic activity.
  • Captopril effectively inhibits hypertensive cardiac hypertrophy.
  • Diltiazem does not inhibit cardiac hypertrophy, and hydralazine may lead to earlier plateauing of hypertrophy.

Related Concept Videos

Pathophysiology of Heart Failure01:17

Pathophysiology of Heart Failure

Heart failure (HF) is a progressive syndrome involving ventricles that leads to inadequate cardiac output. It can be classified based on location and output or ejection fraction. Ejection fraction (EF) is an essential measurement in the diagnosis and surveillance of HF. Reduced EF corresponds to systolic heart failure (HFrEF). However, HF with preserved ejection fraction (HFpEF) is becoming increasingly prevalent. Also known as diastolic HF, this form of HF is related to aging. The...
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...
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...
Cardiomyopathy III: Hypertrophic Cardiomyopathy01:29

Cardiomyopathy III: Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathy, or HCM, is an autosomal dominant genetic disorder characterized by asymmetric left ventricular hypertrophy without ventricular dilation. It is more common in men and is typically diagnosed in young, athletic adults.EtiologyHCM is primarily genetic and is caused by mutations in genes encoding sarcomeric proteins. Researchers have identified over 1400 mutations across at least 11 different genes. Among these, the most frequently occurring mutations are found in the...
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,...
Cellular Adaptation II: Hypertrophy01:26

Cellular Adaptation II: Hypertrophy

Hypertrophy is the increase in the size of individual cells, resulting in the enlargement of a tissue or organ. Unlike hyperplasia, which involves an increase in cell number, hypertrophy is characterized by an increase in cell volume. This process often occurs in response to higher functional demand or hormonal stimulation, leading to the production of more structural proteins and organelles, thereby enhancing the cells' work capacity.There are two primary types of hypertrophy: physiological...