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Renin-Angiotensin Inhibitors and Vascular Effects

  • Chapter
Angiotensin Vol. II

Part of the book series: Handbook of Experimental Pharmacology ((HEP,volume 163 / 2))

  • 192 Accesses

Abstract

Angiotensin II induces vasoconstriction, endothelial dysfunction, vascular inflammation and structural changes that are associated with cell proliferation and hypertrophy as well as fibrosis of the media of vessels. Similar changes occur in experimental and human hypertension. Large and small arteries are remodeled in hypertension, and their structure, function and mechanics are altered. These changes participate in the mechanisms of elevation of blood pressure and in the pathophysiology of its complications. For this reason it has been thought that renin-angiotensin blockade with either angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers could prevent or regress toward normal the vascular changes present in experimental or human hypertension. Changes found in small resistance arteries may be the first manifestation of target organ damage in hypertensive patients. Endothelial dysfunction is often found in vessels from experimental animals and in many patients with elevated blood pressure. Interruption of the renin-angiotensin system may correct many of these abnormalities. Both ACE inhibitors and angiotensin AT1 receptor blockers have been shown to improve vascular structure and endothelial dysfunction in experimental hypertension and in human essential hypertension. In patients, whereas renin-angiotensin blockade corrected vascular changes, the same level of blood pressure lowering with a beta-blocker failed to favorably impact the vasculature. Improved outcomes in clinical trials using ACE inhibitors and angiotensin AT1 receptor antagonists may be a consequence in part of the vascular protective effects offered by these agents

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Schiffrin, E.L. (2004). Renin-Angiotensin Inhibitors and Vascular Effects. In: Angiotensin Vol. II. Handbook of Experimental Pharmacology, vol 163 / 2. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-18497-0_4

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  • DOI: https://doi.org/10.1007/978-3-642-18497-0_4

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