How Can Remodeling Result From Angiotensin?

Cardiac remodeling is a process involving the sympathetic system and the renin-angiotensin-aldosterone system. The activation of both systems leads to cardiac diastolic dysfunction, which is associated with coronary and cardiac tissue remodeling. Angiotensin II (Ang II) regulates cardiac contractility, cell communication, and impulse propagation through specific receptor activation. Risk factors such as hypertension and diabetes can augment the activity and tissue expression of Ang II.

Overexpression of angiotensin-converting enzyme 2 (ACE2) prevents cardiac remodeling and hypertrophy during chronic infusion. Angiotensin II plays a critical role in cardiac remodeling, promoting cardiac myocyte hypertrophy and cardiac fibroblast interstitial fibrotic changes. The aldosterone receptor is a transcriptional factor that induces multiple pathways leading to aldosterone-induced fibrosis. Most patients survive acute myocardial infarction (MI), but this development has drawbacks, including heart failure prevalence.

Ang II initiates tissue remodeling via signaling cascades, inducing SMC hypertrophy, hyperplasia, migration, extracellular matrix production, and synthesis of proinflammatory mediators. An important costimulatory event is the AT1 receptor-dependent activation of NAD(P)H oxidase by Ang II. Studies have indicated that ANG II not only functions as a circulating vasoconstrictor, causing hypertension, but also acts locally as a paracrine and autocrine factor.

Chymase inhibitors have been found to exert cardioprotection in cardiac remodeling. In response to mechanical and/or metabolic stress, the heart undergoes structural remodeling involving cardiomyocyte hypertrophy and myocardial fibrosis. Hypertension is associated with adverse morphologic and functional changes in the cardiovascular system, including remodeling of the left ventricle. Renin-angiotensin system (RAS) is activated in hypertension and may be involved in cardiac hypertrophy and failure.

ACE inhibitors improve the natural history of ventricular remodeling and the syndrome of heart failure.

How does angiotensin cause cardiac remodeling?

Angiotensin II (AII) is a crucial peptide involved in cardiac remodeling, promoting myocyte hypertrophy and cardiac fibroblast interstitial fibrotic changes associated with left ventricular hypertrophy, post myocardial infarction remodeling, and congestive heart failure. AII mediates cardiac hypertrophy directly through the induction of immediate early genes through a MAP kinase dependent pathway, and indirectly by stimulating the release of norepinephrine from cardiac nerve endings and endothelin from endothelial cells.

It also has multiple effects on cardiac fibroblasts, causing cardiac fibroblast proliferation, synthesis and secretion of adhesion molecules and extracellular matrix proteins, and expression of integrin adhesion receptors.

The protective actions of angiotensin converting enzyme inhibitors (ACEI) compared to placebo have been well demonstrated, but their specific mechanisms are not known. The V-HeFT II study showed that enalapril was more effective in preventing heart failure progression than treatment with hydralazine plus isosorbide dinitrate despite similar blood pressure responses. Direct tissue effects have been implicated, and ACE is responsible for catalyzing the degradation of kinins and the conversion of angiotensin I (AI) to angiotensin II (AII).

Ongoing studies of AII’s effects on the cardiovascular system are being vigorously pursued. AII promotes cardiomyocyte hypertrophy, cardiac fibroblast hyperplasia, and interstitial cardiac fibrosis, which increase the volume of the non-myocyte compartment of the heart and are predicted to have a particularly negative impact on the progression of LVH and the globular heart formation associated with post MI remodeling and heart failure.

Factors contributing to cardiac interstitial fibrosis should be recognized, and investigations should address whether approaches that attenuate fibrosis improve ventricular function and remodeling.

How do ACE inhibitors remodel the heart?

ACE inhibitors increase tissue bradykinin accumulation, which has antigrowth effects and reduces vasomotor tone. This increased kinin activation may attenuate structural remodeling in the infarcted heart. Studies have reported that ACE inhibitors attenuated the deterioration of left ventricular function and remodelling in animals with chronic heart failure caused by myocardial infarction (MI). This effect was either blocked by a B2 kinin receptor antagonist or blunted in rats with kininogen deficiency due to spontaneous mutation of the kininogen gene. The mechanism explaining the potential antiremodelling action of bradykinin may relate to increased nitric oxide synthesis or an effect on prostaglandin metabolism.

ACE inhibition decreased blood pressure in WT-MI mice and prevented myocardial remodelling. However, ACE inhibition did not change blood pressure in KO-MI mice. The direct effects of ACE inhibition on the local myocardial renin-angiotensin system may have an important role in preventing myocardial remodelling.

However, the knockout model has a flaw, as the gene being knocked out may regulate a multiplicity of processes outside the targeted gene. In this experiment, chronic hypotension was observed in heterozygous and homozygous mutant mice compared to WT littermates, and renin mRNA in the kidney and plasma renin activity were greatly increased only in the homozygous mutant mice.

What is the action of angiotensin on the heart?

Angiotensin-converting enzyme (ACE) inhibitors are medications that help relax veins and arteries, lowering blood pressure by preventing the body from producing angiotensin 2, a substance that narrows blood vessels, leading to high blood pressure and increased heart work. The best ACE inhibitor depends on various factors, including overall health. Examples of ACE inhibitors include Benazepril, Captopril, Enalapril, Fosinopril, Lisinopril, Moexipril, Perindopril, Quinapril, Ramipril, and Trandolapril.

What is the main cause of cardiac remodeling?

The left ventricle undergoes remodeling due to damage from myocardial infarction or cardiomyopathy, resulting in an enlarged, globular, and thinner ventricle. This remodeling is caused by mechanical stress on the heart muscle. In the early stages of a heart attack, some degree of remodeling can compensate for the damage. However, if the initial remodeling process continues, cardiac function deteriorates and heart failure occurs.

To assess cardiac remodeling, doctors use imaging studies like echocardiography and MRI, which are noninvasive and do not expose patients to radiation. The left ventricular ejection fraction (LVEF) is a useful surrogate measure of remodeling. As the ventricle size increases, its shape becomes more globular, and cardiac muscle function deteriorates, the LVEF worsens. If remodeling improves, the LVEF also improves. These tests allow doctors to follow the extent of remodeling over time.

What is the role of angiotensin converting enzyme in the body?

Angiotensin converting enzyme (ACE) is a crucial enzyme in blood pressure regulation, converting inactive Ang I to active Ang II and degrading active bradykinin. In the 1970s, ACE inhibitors like captopril were developed to treat hypertension, focusing on the production of pressor Ang II. Current research on domain-specific ACE inhibitors is aimed at developing effective hypertension-controlling drugs with fewer side effects.

ACE2 was discovered in 2000, converting Ang II into Ang(1-7), reducing Ang II concentration and increasing Ang(1-7), an essential enzyme for Ang(1-7)/Mas receptor signaling. ACE2 also serves as the lung receptor for the coronavirus causing the severe acute respiratory syndrome (SARS) in 2003.

How do angiotensin converting enzyme inhibitors work?

Angiotensin-converting enzyme (ACE) inhibitors are medications that help relax veins and arteries, lowering blood pressure by preventing the body from producing angiotensin 2, a substance that narrows blood vessels, leading to high blood pressure and increased heart work. The best ACE inhibitor depends on various factors, including overall health. Examples of ACE inhibitors include Benazepril, Captopril, Enalapril, Fosinopril, Lisinopril, Moexipril, Perindopril, Quinapril, Ramipril, and Trandolapril.

What is the role of angiotensin converting enzyme inhibitors in vascular remodeling?

Angiotensin-converting enzyme inhibitors, particularly those with effective tissue penetration, are effective in reversing structural changes, decreasing systemic vascular resistance, and increasing vascular compliance. These drugs are ideal for reducing vascular resistance and improving vascular compliance. Copyright © 2024 Elsevier B. V., its licensors, and contributors. All rights reserved, including text and data mining, AI training, and similar technologies.

What is the action of the angiotensin converting enzyme?

The ACE, also known as angiotensin-converting enzyme, is a crucial part of the renin-angiotensin system (RAS), which regulates blood pressure by regulating fluid volume. It converts angiotensin I into angiotensin II, a vasoconstrictor. The enzyme is found in various parts of the body, including the ileum, testis, and colon. It is also present in the upper lobe of the left lung, heart, and uterine tube.

What is the mechanism of action of angiotensin?

Angiotensin II causes small arteries to constrict, increasing blood pressure. It triggers the adrenal glands to release aldosterone and antidiuretic hormone (ADH), which cause kidneys to retain sodium and potassium. This increases blood volume and blood pressure, completing the renin-angiotensin-aldosterone system. Other hormones, such as corticosteroids, estrogen, and thyroid hormones, also activate this system. Issues in this system can impact blood pressure and sodium and potassium levels. Other factors, such as high cholesterol, genetics, and certain medications, can also affect blood pressure.

How does angiotensin cause vasoconstriction?

The renin-angiotensin-aldosterone system (RAAS) is a crucial regulator of blood volume, electrolyte balance, and systemic vascular resistance. It comprises three significant compounds: renin, angiotensin II, and aldosterone. These compounds elevate arterial pressure in response to decreased renal blood pressure, salt delivery to the distal convoluted tubule, and beta-agonism. The RAAS is ubiquitous and involves multiple organ systems, including the kidneys, lungs, systemic vasculature, adrenal cortex, and brain.

Its function is to regulate vascular tone and salt and water homeostasis, which is essential for cardiac, vascular, and renal physiology. The classical understanding of RAAS has expanded significantly due to discoveries of newer system components over the last few decades.

What is remodelling of the heart?

Cardiac remodelling refers to changes in the heart’s size and shape due to cardiac disease or damage, typically affecting the left ventricle. Doctors can assess this and track its extent over time using imaging studies. Common tests for measuring remodelling are non-invasive and do not expose patients to radiation, allowing for repeated measurements as needed. These tests are often used to monitor the left ventricle’s size, shape, and function.