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• W86551470 abstract "In the early 1970s, ACE inhibition was viewed as an effective means to block the renin-angiotensin component contributing to the maintenance of vasoconstriction [1]. Earlier work had already demonstrated the activation of the renin angiotensin system (RAS) in decompensated congestive heart failure (CHF) [2, 3] and its implications in terms of increased hemodynamic burden to the failing heart. A pilot study using an angiotensin II (Ang II) receptor blocker, saralasin, in a short clinical experiment, demonstrated that Ang II blockade could successfully reverse the hemodynamic aberrations of decompensated CHF, while improving myocardial economy [4]. The decrease in myocardial oxygen consumption resulting from the fall in systemic vascular resistance was, paradoxically, accompanied by an increase in coronary blood flow, a fact that goes against the principles governing the regulation of coronary blood flow. This surprising observation was subsequently explained by the finding that the vasculature of vital organs (heart, kidney and brain) is particularly sensitive to the vasoconstrictive action of Ang II. Consequently, unlike other pharmacological vasodilators, RAS inhibition results in a preferential vasodilation of the coronary, renal and cerebral vasculature, thus maintaining or improving perfusion of vital organs, even in the face of falling systemic blood pressure [5, 6]." @default.
• W86551470 created "2016-06-24" @default.
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• W86551470 date "2001-01-01" @default.
• W86551470 modified "2023-10-03" @default.
• W86551470 title "The role of ACE inhibition in heart failure" @default.
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• W86551470 doi "https://doi.org/10.1007/978-3-0348-7579-0_6" @default.
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