The renin-angiotensin system (RAS) is a hormonal cascade that regulates blood pressure, fluid balance, and electrolyte homeostasis in the body. It begins when the kidneys release the enzyme renin in response to low blood pressure or reduced blood volume; renin acts on angiotensinogen to form angiotensin I, which is …
The renin-angiotensin system (RAS) is a hormonal cascade that regulates blood pressure, fluid balance, and electrolyte homeostasis in the body. It begins when the kidneys release the enzyme renin in response to low blood pressure or reduced blood volume; renin acts on angiotensinogen to form angiotensin I, which is converted by angiotensin-converting enzyme (ACE) into angiotensin II, a potent vasoconstrictor that also stimulates aldosterone release to promote sodium and water retention. Because of its central role in cardiovascular and renal physiology, the RAS is a major target in the management of hypertension, heart failure, and kidney disease, and drugs such as ACE inhibitors and angiotensin-receptor blockers act by interrupting this pathway. Genetic variation in its components, particularly the ACE insertion/deletion polymorphism, has been studied in relation to disease risk. Research in this journal and across related OpenAccessPub titles reflects these themes, including the association of ACE gene polymorphism with hypertension, obesity, and diabetes susceptibility, renal and cardioprotective effects in models of cardiovascular disorder, the efficacy of antihypertensive drug combinations, microRNAs as potential tools in hypertension, and cardiorenal signaling pathways relevant to heart failure and blood-pressure regulation.
12 peer-reviewed articles, ranked by relevance. Each links to its DOI.
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