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Dia-Präsentation von Merck Gesellschaft mbH.
Micardis(R) - MicardisPlus(R) - Hypertonie (38 Abbildungen)
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Zum ersten Bild Abb. 28: Morgendlicher Blutdruck Abb. 29: Blutdrucksenkung - Through/Peak-Ratio Abb. 30: Hypertonie - Behandlung Aktuelles Bild - Abb. 31: Hypertonie - Behandlung Abb. 32: Antihypertensiva - Nebenwirkung Abb. 33: Hypertonie - Behandlung Abb. 34: Antihypertensiva- Eigenschaften Zum letzten Bild
Abbildung 31: Hypertonie - Behandlung
The RAAS, in particular angiotensin II, contributes to cardiovascular disease by increasing blood pressure and also by causing inflammation, leading to sclerosis and tissue hypertrophy. ARBs and angiotensin-converting enzyme (ACE) inhibitors block the RAAS by different mechanisms. ACE inhibitors block the conversion of angiotensin I to angiotensin II. However, angiotensin II can be formed by other pathways. This can lead to a gradual return of angiotensin levels to baseline, a phenomenon termed ‘angiotensin II escape’.1 ACE inhibitors also have other physiological effects, some beneficial,2 but which can also result in cough. Two principal receptors mediate the effects of angiotensin II in humans. The AT1 receptor is responsible for most of the pathological effects associated with angiotensin II, whereas the AT2 receptor counteracts these effects.3 ARBs specifically block the AT1 receptor. Because ARBs specifically block the AT1 receptor but allow continued activation of the AT2 receptor, they can provide tissue-protective effects beyond their effects on blood pressure. 1. Hanon S, et al. Persistent formation of angiotensin II despite treatment with maximally recommended doses of angiotensin converting enzyme inhibitors in patients with chronic heart failure. J Renin Angiotensin Aldosterone Syst 2000; 1: 147–150. 2. Chen R, et al. Important role of nitric oxide in the effect of angiotensin-converting enzyme inhibitor imidapril on vascular injury. Hypertension 2003; 42: 542–547. 3. Hurairah H, Ferro A. The role of the endothelium in the control of vascular function. Int J Clin Pract 2004; 58: 173–183.
 
Hypertonie - Behandlung
Vorheriges Bild Nächstes Bild   


Abbildung 31: Hypertonie - Behandlung
The RAAS, in particular angiotensin II, contributes to cardiovascular disease by increasing blood pressure and also by causing inflammation, leading to sclerosis and tissue hypertrophy. ARBs and angiotensin-converting enzyme (ACE) inhibitors block the RAAS by different mechanisms. ACE inhibitors block the conversion of angiotensin I to angiotensin II. However, angiotensin II can be formed by other pathways. This can lead to a gradual return of angiotensin levels to baseline, a phenomenon termed ‘angiotensin II escape’.1 ACE inhibitors also have other physiological effects, some beneficial,2 but which can also result in cough. Two principal receptors mediate the effects of angiotensin II in humans. The AT1 receptor is responsible for most of the pathological effects associated with angiotensin II, whereas the AT2 receptor counteracts these effects.3 ARBs specifically block the AT1 receptor. Because ARBs specifically block the AT1 receptor but allow continued activation of the AT2 receptor, they can provide tissue-protective effects beyond their effects on blood pressure. 1. Hanon S, et al. Persistent formation of angiotensin II despite treatment with maximally recommended doses of angiotensin converting enzyme inhibitors in patients with chronic heart failure. J Renin Angiotensin Aldosterone Syst 2000; 1: 147–150. 2. Chen R, et al. Important role of nitric oxide in the effect of angiotensin-converting enzyme inhibitor imidapril on vascular injury. Hypertension 2003; 42: 542–547. 3. Hurairah H, Ferro A. The role of the endothelium in the control of vascular function. Int J Clin Pract 2004; 58: 173–183.
 
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