Effects of chronic sympatho-inhibition on renal excretory function in XXXX .

@entity23189 @entity101 @entity1219 @entity2792 @entity95 @entity1372 @entity2791 @entity177 @entity551
OBJECTIVE: Treatment of @entity2792 with drugs that directly target the renin-angiotensin system may compromise glomerular filtration and renal excretory function, leading to @entity177 . Centrally acting sympathoinhibitory agents also inhibit the renin-angiotensin system, so we determined whether this treatment modality alters renal excretory function in @entity95 with @entity2792 . METHODS: @entity95 were equipped with bilateral renal artery flow probes and a renal nerve electrode. @entity101 was induced with a renal artery clip (2K1C) or @entity95 were sham-clipped. After 2 weeks, a subcutaneous minipump was implanted to deliver @entity23189 (2.5 mg/kg per day) or vehicle for 3 weeks. Haemodynamic variables and renal function were studied under control conditions and during intravenous infusion of isotonic saline (154 mmol/l @entity1219 ) at increasing rates of 4, 12 and 36 ml/kg per hour. RESULTS: @entity551 ( @entity551 ) and renal sympathetic nerve activity (RSNA) were greater in 2K1C @entity95 than sham-clipped @entity95 , but total urine flow, @entity1372 excretion and glomerular filtration rate were similar in the two groups. In 2K1C @entity95 , @entity23189 reduced @entity551 to close to control levels and reduced RSNA (40%), but did not significantly alter basal renal blood flow, glomerular filtration rate, urine flow or @entity1372 excretion. The natriuretic response to isotonic saline load in 2K1C @entity95 was not significantly altered by @entity23189 . CONCLUSION: These observations show that chronic treatment of @entity95 with @entity2791 with a centrally acting sympathoinhibitory agent, despite normalizing @entity551 , does not compromise renal excretory function. Thus, this treatment modality may be particularly useful in @entity2792 .
