The renin-angiotensin-aldosterone system (RAAS) - physiology and molecular mechanisms of functioning.
Secretion of renin juxtaglomerular cells into bloodstream initiates activation of an enzymatic-hormonal cascade known as the RAAS (renin - angiotensin - aldosterone system). As a result, blood pressure is increased by the means several interrelated mechanisms. Mechanism of Zjednoczoaction of this system has been known for decades, but a few previously unknown components were recently added, such as ACE-2 and Ang(1-7), and their role often seems to be opposite to that of the conventional components. Local tissue systems also have important biological functions. They operate largely independently of the systemic activity, and their activity is observed primarily in the kidney, heart, in blood vessels, adrenal gland and nervous system. Angiotensin-2 (Ang-2), the main RAAS effector, has a wide scope of action, and thus abnormalities in its functioning have many consequences. Excessive activation is accompanied by chronic inflammation, as Ang-2 stimulates inflammatory mediators. As a result, degenerative processes and atherosclerosis are initiated. RAAS imbalance is associated with the most common diseases of civilization, such as cardio-vascular diseases, diabetes, kidney diseases, preeclampsia, osteoporosis and even neurodegenerative diseases. Many of these pathological processes are attributed to the excessive activation of tissue RA system. Therapeutic strategies based on inhibition of the RAAS are commonly used mainly in the treatment of hypertension and other cardiovascular disorders. The benefits of this class of drugs is primarily a decrease in blood pressure, but also the suppression of inflammatory processes and other pathological phenomena resulting from excessive activation of the RAAS. For that reason, some consider to use RAAS inhibitors in other diseases, e.g. Parkinson's disease. Further studies give hope for the improvement of RAAS inhibitor therapy and the development of new therapeutic strategies.
Laboratorium Immunogenetyki Klinicznej i Farmakogenetyki, Instytut Immunologii i Terapii Doświadczalnej im. L. Hirszfelda Polskiej Akademii Nauk we Wrocławiu.
Monika
M
Chaszczewska-Markowska
Laboratorium Immunogenetyki Klinicznej i Farmakogenetyki, Instytut Immunologii i Terapii Doświadczalnej im. L. Hirszfelda Polskiej Akademii Nauk we Wrocławiu.
Maria
M
Sagan
Laboratorium Immunogenetyki Klinicznej i Farmakogenetyki, Instytut Immunologii i Terapii Doświadczalnej im. L. Hirszfelda Polskiej Akademii Nauk we Wrocławiu; Katedra i Klinika Chorób Wewnętrznych, Zawodowych, Nadciśnienia Tętniczego i Onkologii Klinicznej, Uniwersytet Medyczny im. Piastów Śląskich we Wrocławiu.
Katarzyna
K
Bogunia-Kubik