By Murat Bas
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Violent clash in sub-Saharan Africa has been liable for the direct and oblique deaths of thousands of civilians and has contributed considerably to the low degrees of human defense within the zone. The international locations of sub-Saharan Africa which have been embroiled in violent clash are characterized through abject poverty, insufficient provider provision, political instability, retarded fiscal development and different demanding situations to total improvement that deter the enhancement of human safeguard.
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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 ). 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.