Endothelin role in the orthostatic stress

Abstract

Orthostasis adoption causes hemodynamic changes. Hydrostatic opposition to the venous return, venous return reduction and cardiac output decrease act as stimuli and generate compensatory mechanisms. The central nervous system adjusts the autonomic sympathetic and parasympathetic activity. The autonomous nervous system causes a tonic and reflexive influence on the main variables of the cardiovascular system and, together with hormonal components, extends the adaptation capacity in face of postural changes. Any difficulties in this compensatory mechanism that prevents it from functioning properly may result in hypotension response failure, what, on its turn, can lead to cerebral hypoperfusion, hypoxia and loss of consciousness. Blood pressure maintenance at normal levels is important for the internal medium homeosthasis. Baroreflex plays an important role in the cardiovascular control in the short-term in the adaptation of the orthostatic stress, preventing excessive blood pressure alterations. During the orthostatic stress, neuroendocrinal changes also occur as alteration in endothelin plasma levels. Endothelin, a peptide formed by 21 amino acids, shows a powerful vasoconstrictor action. It also demonstrates that its levels in the blood are increased in response to an orthostatic stress. However, although endothelin-1 levels increase in response to an acute postural stress, its role in cardiovascular homeosthasis and its relation in the release of other hormones are still controversial and quite unknown in humans in vivo.