Synthesis, anti-bacterial and anti-protozoal activities of amidinobenzimidazole derivatives and their interactions with DNA and RNA.

Amidinobenzimidazole derivatives connected to 1-aryl-substituted 1,2,3-triazole through phenoxymethylene linkers 7a-7e, 8a-8e, and 9a-9e were designed and synthesised with the aim of evaluating their anti-bacterial and anti-trypanosomal activities and DNA/RNA binding affinity. Results from anti-bacterial evaluations of antibiotic-resistant pathogenic bacteria revealed that both o-chlorophenyl-1,2,3-triazole and N-isopropylamidine moieties in 8c led to strong inhibitory activity against resistant Gram-positive bacteria, particularly the MRSA strain. Furthermore, the non-substituted amidine and phenyl ring in 7a induced a marked anti-bacterial effect, with potency against ESBL-producing Gram-negative E. coli better than those of the antibiotics ceftazidime and ciprofloxacin. UV-Vis and CD spectroscopy, as well as thermal denaturation assays, indicated that compounds 7a and 8c showed also binding affinities towards ctDNA. Anti-trypanosomal evaluations showed that the p-methoxyphenyl-1,2,3-triazole moiety in 7b and 9b enhanced inhibitory activity against T. brucei, with 8b being more potent than nifurtimox, and having minimal toxicity towards mammalian cells

Renin- angiotensin system in control of vascular reactivity

This paper aimed to present recent knowledge of the role of the renin-angiotensin system (RAS) in the control of vascular relaxation mechanisms and the relation to development and maintenance of hypertension. The emphasisis given on the role of oxidative stress and NO – dependent and prostanoid - dependent vascular relaxation mechanisms that are impaired in SS salt-sensitive rat strain (that exhibit chronically low plasma renin activity), and restored in consomic SS.13BN rats (that have chromosome 13, containing renin gene, introgressed from BN rat into SS genetic background). In conclusion, results of numerous experimental studies suggest that hypoactive (as well as hyperactive) RAS may contribute to development and maintenance of hypertension due to the effects of angiotensin II on vascular reactivity