Effects of XXXX inhibition on renal regulation of salt and water.

@entity1369 @entity1289 @entity5704 @entity1372 @entity1483 @entity177 @entity2629 @entity551 @entity2753 @entity6085
CHF may activate the RAS by various mechanisms. Acute CHF is associated with high PRA, whereas chronic, stable disease is combined with normal values. The response to ACEI is affected by blood pressure, degree of activation of the RAS, salt balance and degree of possible @entity177 . It may also be affected by concomitant diuretic or, e.g., digoxin therapy. ACEI improves RPF, GFR may remain normal or may increase, if it was previously impaired due to reduced RPF. Severe @entity551 in combination with decreased autoregulatory capacity may decrease GFR. Generally, renal excretion of @entity1372 and water increase. These changes in renal handling of salt and water are primarily caused by decreased @entity5704 . They are also augmented by inhibited sympathetic tone and thirst and decreased release of @entity6085 and @entity1369 . Increased synthesis of vasodilating and natriuretic PGs is probably also of some importance. Dilutional @entity2753 may be corrected by combined @entity1289 inhibitor and @entity1483 treatment. Water and @entity1372 excretion increase and @entity1372 is redistributed from the intracellular space. Low serum @entity1372 values increase and @entity2629 may be corrected, if @entity1289 inhibitor doses are carefully titrated to avoid severe @entity551 . These effects are ascribed mainly to a decrease of @entity5704 , thirst and @entity6085 release. The effect of @entity1483 is improved since increased amounts of salt are delivered to the loop of Henle and access of @entity1483 to its site of action is facilitated by increased RPF. ACEI does not cause any obvious negative effects on renal handling of salt and water.(ABSTRACT TRUNCATED AT 250 WORDS)
