Titlebook: Angiotensin and the Heart; H. Grobecker,Gerd Heusch,B. E. Strauer Book 1993 Dr. Dietrich Steinkopff Verlag GmbH & Co. KG, Darmstadt 1993 A

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https://doi.org/10.1007/978-3-030-69583-5ddition, cardiac RAS may contribute to the pathophysiology of heart failure. Experimental and clinical studies with ACE inhibitors point to a role for tissue ACE activity in the development of atherosclerosis, as well as cardiac hypertrophy and remodeling.

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https://doi.org/10.1007/978-3-030-54001-2derived vasodilator system. Angiotensin II not only can activate vascular smooth muscle cells (where it causes contraction and proliferation), but also endothelial cells. In certain blood vessels, angiotensin II can stimulate prostacyclin production; in addition, angiotensin II activates endothelin

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https://doi.org/10.1007/978-3-030-54001-2ncreases to match the increased oxygen consumption, α-adrenergic coronary constriction remains operative in ischemic myocardium, thus precipitating or contributing to acute myocardial ischemia during sympathetic activation and exercise in experimental animals as well as in patients with stable angin

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https://doi.org/10.1007/978-3-030-54001-2schemia at rest and during exercise, a significant fraction of about 30% of normotensive patients with CAD does not benefit or even deteriorates. Lowering of coronary perfusion pressure and alteration of transmural blood flow distribution may be responsible for this. In patients with left ventricula