Abstract
There is no doubt that in patients with endstage renal failure sodium/water retention and (often unrecognized) hypervolaemia is the single most important determinant for elevated blood pressure. More detailed analysis reveals that in the renal patient susceptibility to hypervolaemia is increased due to inappropriately elevated activity of pressor systems (and/or decreased activity of depressor systems). These abnormalities comprise inappropriately activated renin-angiotensin system (RAS) (circulating and local) as well as sympathetic activity, but more hypothetical possibilities must also be considered, e.g. abnormalities of renal vasodilators (medullipin), L-arginine-derived agmatin, endothelin and NO.
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