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Dia-Präsentation von Merck Gesellschaft mbH.
ONTARGET - Ongoing telmisartan alone and in combination with ramipril global endpoint trial und TRANSCEND - Telmisartan randomized assessment study in ACE-I intolerant subjects with cardiovascular disease (30 Abbildungen)
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Zum ersten Bild Abb. 7: ONTARGET - the HOPE study Abb. 8: HOPE study results: primary end point Abb. 9: HOPE study results: secondary end point Aktuelles Bild - Abb. 10: ONTARGET - Rationale Abb. 11: ONTARGET - rationale Abb. 12: ONTARGET - rationale Abb. 13: ONTARGET - objectives Zum letzten Bild
Abbildung 10: ONTARGET - Rationale
ARBs exert their antihypertensive effects by selectively blocking the angiotensin II type 1 (AT1) receptors. This receptor subtype mediates most of the negative cardiovascular effects of its substrate, angiotensin II, including vasoconstriction, sodium and water retention, sympathetic nervous system activation and growth-promoting effects. Importantly, ARBs do not block type 2 (AT2) receptors, which are responsible for many of the beneficial effects of angiotensin II, such as tissue regeneration and the inhibition of inappropriate cell proliferation. ACE inhibitors mediate an antihypertensive effect earlier in the renin–angiotensin cascade, preventing the conversion of angiotensin I to angiotensin II. ACE is also a kininase and is involved in the catabolism of various kinin peptides such as bradykinin. As a consequence of ACE inhibition, plasma levels of bradykinin increase. Bradykinin is associated with beneficial vasodilatory and tissue protective effects.
 
ONTARGET - Rationale
Vorheriges Bild Nächstes Bild   


Abbildung 10: ONTARGET - Rationale
ARBs exert their antihypertensive effects by selectively blocking the angiotensin II type 1 (AT1) receptors. This receptor subtype mediates most of the negative cardiovascular effects of its substrate, angiotensin II, including vasoconstriction, sodium and water retention, sympathetic nervous system activation and growth-promoting effects. Importantly, ARBs do not block type 2 (AT2) receptors, which are responsible for many of the beneficial effects of angiotensin II, such as tissue regeneration and the inhibition of inappropriate cell proliferation. ACE inhibitors mediate an antihypertensive effect earlier in the renin–angiotensin cascade, preventing the conversion of angiotensin I to angiotensin II. ACE is also a kininase and is involved in the catabolism of various kinin peptides such as bradykinin. As a consequence of ACE inhibition, plasma levels of bradykinin increase. Bradykinin is associated with beneficial vasodilatory and tissue protective effects.
 
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