Download Angioedema congress book : 3 tables by Murat Bas PDF

By Murat Bas

ISBN-10: 3131474211

ISBN-13: 9783131474216

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Immunopharmacology 1996; 33: 341 – 333 5 Sharma JN, Uma K, Yusof AP. Left ventricular hypertrophy and its relation to the cardiac kinin-forming system in hypertensive and diabetic rats. Int J Cardiol 1998; 63: 229 – 235 6 Nustad K, Vaaje K, Pierce JV. Synthesis of kallikreins by rat kidney slices. Br J Pharmacol 1975; 53: 229 – 234 7 Clements J, Hooper J, Dong Y, Harvey T. The expanded human kallikrein (KLK) gene family: genomic organisation, tissue-specific expression and potential functions. Biol Chem 2001; 382: 5 – 14 8 Fleming I.

Effects of angiotensin-converting enzyme inhibitors and angiotensin II type 1 receptor antagonists in rats with heart failure. J Clin Invest 1997; 99: 1926 – 1935 10 Yang XP, Liu YH, Metha D, Cavasin MA, Shesely E, Xu J, Liu F, Carretero OA. Diminished cardioprotective response to inhibition of angiotensin-converting enzyme and angiotensin II type 1 receptor in B2 kinin receptor gene knockout mice. Circ Res 2001; 88: 1072 – 1079 11 Nussberger J, Koike H. Antagonizing the angiotensin II subtype 1 receptor: a focus on olmesartan medoxomil.

The inhibition of ACE is at the center of discussion (reviewed in [1]). ACE symbolizes the close physiological and pathophysiological relationships between the renin-angiotensin system (RAS) and the kallikreinkinin system (KKS) since it is, on the one hand, essential for the formation of angiotensin II (ANG II) from angiotensin I (ANG I) and, on the other hand, mainly responsible for the inactivation of bradykinin. The physiological activities that ANG II mediates via the AT1 receptor and that bradykinin medi- ates via the B2 receptor are often antagonistic and the KKS can rightly be considered as the physiological opposite of the RAS (Figs.

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