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Introduction Heart failure (HF) is a complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the pumping capacity of the heart. A variety of compensatory mechanisms are activated, including the adrenergic nervous system, the renin-angiotensin-aldosterone system (RAAS) and the cytokine system, all of which have been extensively studied. However, there is little information on the participation of the kallikrein-kinin system (KKS), in HF. Kallikreins (EC 3.4.21.8) are key—enzymes in the KKS, constituting a subgroup of the serine protease family known to have several physiological functions. The kallikreins are found in glandular cells, neutrophils and biological fluids and can be divided into two main groups: plasma (EC 3.4.21.3 4) and tissue (EC 3.4.21.35) kallikreins. The KLK1 gene, located on chromosome 19q13.4, expresses human tissue kallikrein (hK1), the principal known biochemical function of which is releasing the vasoactive and spasmogenic decapeptide kalli-din (Lys-bradykinin) (Lys-BK) from the plasma protein low-molecular-weigh kininogen. The KLK1 gene expression is highest in the pancreas, kidney and salivary glands, but also in prostate, breast, testis, uterus, heart and central nervous system. Renal kallikrein is believed to release kinins in the distal nephron. Accumulative evidence suggests that renal KKS may play a role in the regulation of renal function and in certain diseases such as hypertension. The role of KKS in HF is not clear yet.

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2008-06-03   |   1,121 visitas   |   Evalua este artículo 0 valoraciones

Vol. 3 Núm.1. Enero-Marzo 2008 Pags. 32-35 Rev Insuf Cardíaca 2008; III(1)