The Renin—Angiotensin—Aldosterone System
Giuseppe Mancia, Guido Grassi, Konstantinos P. Tsioufis, Anna F. Dominiczak, Enrico Agabiti Rosei in Manual of Hypertension of the European Society of Hypertension, 2019
Regarding Ang II actions in the heart, it is well documented that Ang II via the AT1R promotes cardiac hypertrophy, which is mainly due to cardiomyocyte hypertrophy (64). Cardiac hypertrophy develops as a reaction to chronically elevated intracardiac pressure (due to hypertension or as a result of stenosis of the cardiac valves or the big, afferent blood vessels). Cardiac hypertrophy is a compensatory mechanism, which in earlier stages preserves cardiac function. However, an excess of hypertrophy leads to decompensation, resulting in cardiac failure and increased mortality (65). Several mechanisms lead to a deterioration of cardiac function due to enhanced Ang II production, among them impaired diastolic calcium handling (66), cardiac fibrosis (67), impaired diastolic relaxation due to disturbed sarcoplasmic reticulum calcium pump activity (68) and also arrhythmias (69).
Endothelin and Cardiac Hypertrophy
Malcolm J. Lewis, Ajay M. Shah in Endothelial Modulation of Cardiac Function, 2020
Cardiac hypertrophy is a commonly observed complication of a variety of cardiovascular diseases including hypertensive and ischemic heart disease and cardiomyopathies. The nature of the hypertrophic response of the heart is a compensatory one to counter the increased afterload or disturbed function of the heart. However, when this physiological response progresses beyond a certain point, a variety of dysfunctions accompany cardiac hypertrophy (Shepherd et al., 1989). Diastolic dysfunction is one of the most common manifestations of cardiac hypertrophy, which in turn may lead to congestive heart failure due to increased filling pressure. Subsequently, disturbance of systolic function and congestive heart failure may occur late in the evolution of cardiac hypertrophy. In addition, a variety of ventricular arrhythmias may also accompany the development of cardiac hypertrophy. Thus the prevention of cardiac hypertrophy is one of the most important problems that should be targeted by both clinical and basic researchers in cardiology.
Cardiac Performance During Diabetes
Grant N. Pierce, Robert E. Beamish, Naranjan S. Dhalla in Heart Dysfunction in Diabetes, 2019
Blood pressure measurements will, of course, be dependent upon the presence of atherosclerotic complications in the arterial system during diabetes. Hypertension in the diabetic population has been reported.6 In relatively asymptomatic diabetic men, systolic blood pressure tended to be higher in those patients with autonomic neuropathy but lower in diabetics considered to have peripheral neuropathy.4 Diastolic blood pressure changes may correlate with pathological alterations in heart morphology. Shapiro and colleagues7 discovered that the posterior wall of the heart was thicker in diabetic patients if the diastolic blood pressure was between 100 to 125 mmHg than if it was less than 100 mmHg. Cardiac hypertrophy has been considered as an indicator of clinical heart disease.8
Andrographolide contributes to the attenuation of cardiac hypertrophy by suppressing endoplasmic reticulum stress
Published in Pharmaceutical Biology, 2023
Qingxin Tian, Jianlong Liu, Qin Chen, Mingxiao Zhang
Cardiac hypertrophy refers to a response of the heart to augmented workload, such as dilated cardiomyopathy, aortic stenosis and hypertension (Myers et al. 2017). Pathological cardiac hypertrophy is characterized by enlarged cardiomyocytes and obstructed contractility of the heart, accompanied by internal changes in cardiomyocytes, including apoptosis, cardiac fibrosis, metabolism and gene expression (Tham et al. 2015; Gesmundo et al. 2017). In the case of coronary artery disease, valvular heart disease and hypertension, the heart may also become hypertrophic under chronic stress or volume overload (Weeks and McMullen 2011). Moreover, cardiac hypertrophy has been reported to usually develop into heart failure (Shimizu and Minamino 2016). Several researchers have clarified that multiple signalling pathways are involved in the occurrence of cardiac hypertrophy, such as typical G protein-coupled receptor (GPCR) and calcineurin-activated T nuclear factor (NFAT) signalling pathways (Madukwe et al. 2018; Zhang et al. 2020). Nevertheless, the mortality from heart failure remains high due to the complex mechanism of the transition from hypertrophy to heart failure, as well as the difficulty of reversing cardiac hypertrophy. Therefore, it is urgent to find a new pharmacological drug that can suppress the progression of cardiac hypertrophy.
Effects of berberine hydrochloride on left ventricular structure and function in rats with myocardial hypertrophy
Published in Acta Cardiologica, 2023
Tuli Kou, Haorou Luo, Yang Shen, Ye Su, Lixue Yin
Cardiac remodelling is an essential pathological mechanism in the process of heart failure. Cardiac hypertrophy plays a vital role in cardiac remodelling. It is a critical stage in the development of cardiac structure and function from compensation to decompensation, as well as an independent risk factor for the increased prevalence and mortality of cardiovascular diseases [1]. Early detection and treatment of cardiac hypertrophy are critical. Rho/ROCK signalling pathway plays an essential role in the development of cardiovascular diseases. Overexpression of Rho and ROCK can aggravate cardiac hypertrophy; inhibition of Rho/ROCK signalling pathway-related proteins can effectively alleviate left ventricular hypertrophy and prevent cardiac remodelling from progressing to heart failure [2–4]. BBR is a natural plant alkaloid that can inhibit pathological cardiac hypertrophy by up to 50% [5–7]. However, whether berberine hydrochloride can improve cardiac hypertrophy by regulating the Rho/ROCK signalling pathway is unclear. 2D-STE is a relatively new detection technology, which is more accurate than traditional echocardiography in the early detection of abnormal changes in cardiac function [8–11]. There are few studies on applying 2 D-STE in evaluating left ventricular function in rat models of myocardial hypertrophy.
Dendrobium candidum aqueous extract attenuates isoproterenol-induced cardiac hypertrophy through the ERK signalling pathway
Published in Pharmaceutical Biology, 2020
Yuan-Yuan Cao, Ke Li, Ying Li, Xiao-Ting Tian, Hui-Xue Ba, Aiping Wang, Xiao-Hui Li
Pathological myocardial hypertrophy is a decompensated response of the myocardial tissue to sustained load increase, which is usually caused by sympathetic nervous excitement and hypertension. Cardiac hypertrophy is also an independent risk factor for ischaemic heart disease, arrhythmia, and sudden cardiac death. Preventing the development of cardiac hypertrophy is conducive to reducing cardiovascular events. The mechanism of cardiac hypertrophy is extremely complicated (Tham et al. 2015). It has been reported that multiple pathogens can activate intracellular signalling transduction pathways, such as the ERK1/2 signalling pathway, leading to a series of biological reactions participating in cardiac hypertrophy (Bernardo et al. 2010). Several medications including angiotensin converting enzyme inhibitors (ACEI) and calcium channel blockers (CCBs) have been used clinically. However, the high mortality rate of patients necessitates more effective therapeutic and protective medications (Tham et al. 2015).
Related Knowledge Centers
- Concentric Hypertrophy
- Left Ventricular Hypertrophy
- Myocardial Infarction
- Phenotype
- Right Ventricular Hypertrophy
- Shortness of Breath
- Ventricle
- Heart
- Hypertrophy
- Ventricular REModeling
- Shortness of Breath