@entity916 -angiotensin system promotes @entity1372 and @entity2865 retention, participates in the defense response to @entity3485 and, in @entity712 , contributes to @entity4 formation and progression of the disease. We investigated whether @entity1289 -inhibitors interfere with the action of the @entity916 -angiotensin system on the nephron, and therefore with water and urinary electrolytes excretion. The interaction among @entity916 -angiotensin system, diuretic treatment and urinary electrolytes was evaluated both during chronic treatment and in response to acute @entity916 -angiotensin system activation as that observed after extracorporeal ultrafiltration-induced transient @entity3485 . Plasma @entity916 activity and @entity1369 , body fluid balance and urinary @entity1372 , @entity2865 and @entity972 concentrations were evaluated in 30 @entity1 with @entity712 in NYHA II-III functional class, grouped according to whether long-term therapy did not include (Group I, n = 15) or included (Group II, n = 18) @entity1289 -inhibitors. All parameters were evaluated at baseline and after a single session of extracorporeal ultrafiltration. At baseline, urinary output and urinary @entity1372 and @entity2865 concentrations were similar in the two groups, while urinary @entity972 concentration was lower in @entity1 assuming @entity1289 -inhibitors (Group II). Plasma @entity916 activity was higher and @entity1369 was lower in Group II than in Group I. After removal of similar amounts of plasma water by extracorporeal ultrafiltration, body weight decreased in both groups but the decrease was maintained in the following days only in Group II @entity1 . A transient reduction (48 hours) of both plasma volume and urinary output was observed after ultrafiltration in both groups. Despite plasma @entity916 activity and @entity1369 increase, urinary electrolytes response to ultrafiltration was different in the two groups: @entity1372 and @entity2865 were reduced, and @entity972 did not change in Group 1 while, in Group II, @entity1372 and @entity2865 did not change and @entity972 excretion was significantly increased. In conclusion, chronic treatment with @entity1289 -inhibitors does not enhance the excretion of @entity1372 in @entity712 but just mitigates @entity972 loss. The role of these drugs becomes particularly relevant during acute @entity916 -angiotensin system activation due to @entity3485 ; in this setting @entity1289 -inhibitors counteract @entity1372 and @entity2865 retention resulting in a potential hazard due to interference with the defence mechanisms toward @entity3485 , and an amplification of extracorporeal ultrafiltration efficacy by preventing @entity4 recovery after its mechanical removal.

[The influence of @entity1289 inhibitors on urinary electrolyte secretion and the response to transitory @entity3485 in XXXX ].

@entity1 :: ('9606', 'Species') :: ['patients'] @entity972 :: ('MESH:D011188', 'Chemical') :: ['potassium'] @entity712 :: ('MESH:D006333', 'Disease') :: ['congestive heart failure'] @entity1289 :: ('1636', 'Gene') :: ['ACE'] @entity1369 :: ('MESH:D000450', 'Chemical') :: ['aldosterone'] @entity4 :: ('MESH:D004487', 'Disease') :: ['edema'] @entity1372 :: ('MESH:D012964', 'Chemical') :: ['sodium'] @entity3485 :: ('MESH:D020896', 'Disease') :: ['hypovolemia'] @entity2865 :: ('CHEBI:17996', 'Chemical') :: ['chloride'] @entity916 :: ('5972', 'Gene') :: ['Renin', 'renin']
@entity712 :: (MESH:D006333,Disease) :: ['chronic heart failure']
