Angiotensin II Contributes to the Pathophysiology of Heart Failure

Angiotensin is a protein hormone; it is a part of the renin-angiotensin system (RAS), that causes blood vessels to become narrower, helps to maintain blood pressure and fluid balance in the body. It is the primary effector hormone that secreted in response to physiological stimuli. Despite, there is now general agreement that RAS is known to be much more complicated, acting locally within organs or tissue, through both intracrine and autocrine/paracrine mechanisms and systemically, to exert its effects on target organs, including the heart. High secretion of angiotensin II is a common problem resulting in excess fluid retained by the body and, ultimately, raised blood pressure frequency occurs in heart failure where angiotensin is also thought to take part in growing the heart size. Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers are used in the clinic to avoid these adverse effects. Besides, High levels of Ang II often causes hypertension, renal failure, and cardiac fibrosis. In this review, will be illustrated how Chronic Activation of the renin-angiotensin System Induces heart failure and injures endothelial cells by activation of cellular suicide pathways leading to apoptosis. Its Effects mediated by angiotensin II receptor (AT2) are suggested to include inhibition of cell growth, fetal tissue progression, extracellular matrix modulation, neuronal regeneration, cellular differentiation, apoptosis, and may be vasodilation and left ventricular hypertrophy.