RGD Reference Report - Effect of valsartan versus lisinopril on peritoneal sclerosis in rats. - Rat Genome Database

RGD Reference Report - Effect of valsartan versus lisinopril on peritoneal sclerosis in rats. - Rat Genome Database

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Effect of valsartan versus lisinopril on peritoneal sclerosis in rats.
Authors:	Duman, S Sen, S Duman, C Oreopoulos, D G
Citation:	Duman S, etal., Int J Artif Organs. 2005 Feb;28(2):156-63.
RGD ID:	12879430
Pubmed:	PMID:15770604 (View Abstract at PubMed)
BACKGROUND: Peritoneal sclerosis (PS) is one of the most serious causes of failure in long-term peritoneal dialysis. Angiotensin II is known to promote fibrosis and inflammation in various tissues. We previously showed that ACE inhibitors (ACEIs) have beneficial effects on hypertonic PD solutions (3.86% PD) induced peritoneal alterations. The aim of this study is to compare the effects of an ACEI and a receptor blocker on peritoneal alterations induced by hypertonic PD solutions in rats. METHODS: Forty-three non-uremic rats were divided into four groups: group I (Sham) rats received no treatment (n=11), group II received hypertonic (3.86%, 10 ml/day) PD solution (n = 10) and groups III and IV received hypertonic PD solution (10 ml/day) plus 640 mg/L valsartan (n=11) and 100 mg/L lisinopril in drinking water (n = 11). After four weeks, a one-hour peritoneal equilibration test (PET) was performed with 3.86% PD solution. Dialysate-to-plasma urea ratio (D/P urea), glucose reabsorption (D 1 /D 0 glucose), ultrafiltration volume (UF), dialysate protein, TGFbeta 1 and VEGF levels were determined. RESULTS: Administration of valsartan or lisinopril resulted in preserved UF (8+/-0.8 and 6.7+/-0.7 vs 4.9+/-0.8 mL), D1/D0 glucose (0.69+/-0.05 and 0.62+/-0.05 vs 0.56+/-0.04) and peritoneal thickness (19.4+/-2.9 and 28.5+/-5.2 vs 53+/-3 microm), respectively. Both higher level of TGF beta 1 (206+/-40 vs 474+/-120 pg/mL, p<0.05), and VEGF in dialysate effluent (4+/-0.4 vs 7.9+/-3 pg/mL, p>0.05), was determined in the dextrose group. Both cytokines are partially inhibited by valsartan or lisinopril (p >0.05) CONCLUSION: Exposure to hypertonic glucose solution resulted in alterations in peritoneal transport manifested by a rapid dissipation of the glucose gradient and resultant impaired UF response. Administration of valsartan or lisinopril led to attenuation of these alterations. We suggest that the equal protection of the peritoneal membrane from the effects of hypertonic glucose was achieved by receptor blockers and ACE inhibitors.

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Object Symbol	Species	Term	Qualifier	Evidence	With	Notes	Source	Original Reference(s)
ACE	Human	Peritoneal Fibrosis	treatment	ISO	Ace (Rattus norvegicus)		RGD
Ace	Rat	Peritoneal Fibrosis	treatment	IMP			RGD
Ace	Mouse	Peritoneal Fibrosis	treatment	ISO	Ace (Rattus norvegicus)		RGD

Genes (Rattus norvegicus)


Ace (angiotensin I converting enzyme)

Genes (Mus musculus)


Ace (angiotensin I converting enzyme)

Genes (Homo sapiens)


ACE (angiotensin I converting enzyme)