1. The kallikrein-kinin system has a significant role in regulating arterial blood pressure. 2. Reduced formation of the kinin compontents may cause hypertensive diseases. This is because of the fact that this system is responsible for vasodilatation, reduction in total peripheral resistance, natriuresis, diuresis, increasing renal blood flow and releasing various vasodilator agents. 3. Reduced kinin-kallikrein generation in hypertensive subjects may also be associated with genetic and environmental defects. 4. The kallikrein-kinin system when administered to hypertensive patients can lower their raised blood pressure to normotensive levels. 5. The mode of action of angiotensin-converting enzyme inhibitors principally may be dependent on the kinin system protection.
We investigated the cardiac tissue kallikrein and kininogen levels, left ventricular wall thickness and mean arterial blood pressure of Wistar Kyoto and spontaneously hypertensive rats with and without streptozotocin-induced diabetes. The mean arterial blood pressure was highly elevated (P<0.001) in Wistar Kyoto diabetic and spontaneously hypertensive diabetic rats as compared with their respective controls. The cardiac tissue kallikrein and kininogen levels were reduced significantly (P<0.001) in diabetic Wistar Kyoto, spontaneously hypertensive and diabetic spontaneously hypertensive compared with Wistar Kyoto control rats. In addition, the left ventricular thickness was found to be increased (P<0.001) in diabetic Wistar Kyoto and spontaneously hypertensive rats in the presence and in the absence of diabetes. Our results indicate that reduced activity of the kinin-forming system may be responsible for inducing left ventricular hypertrophy in the presence of raised mean arterial blood pressure in diabetic and hypertensive rats. Thus, the kinin-forming components might have a protective role against the development of left ventricular hypertrophy. The possible significance of these findings is discussed.
Microbial fuel cell (MFC) is a promising technology that utilizes exoelectrogens cultivated in the form of biofilm to generate power from various types of sources supplied. A metal-reducing pathway is utilized by these organisms to transfer electrons obtained from the metabolism of substrate from anaerobic respiration extracellularly. A widely established model organism that is capable of extracellular electron transfer (EET) is Shewanella oneidensis. This review highlights the strategies used in the transformation of S. oneidensis and the recent development of MFC in terms of intervention through genetic modifications. S. oneidensis was genetically engineered for several aims including the study on the underlying mechanisms of EET, and the enhancement of power generation and wastewater treating potential when used in an MFC. Through engineering S. oneidensis, genes responsible for EET are identified and strategies on enhancing the EET efficiency are studied. Overexpressing genes related to EET to enhance biofilm formation, mediator biosynthesis, and respiration appears as one of the common approaches.