Ultrastructural changes in the remnant kidney (after 5/6 nephrectomy) glomerulus after losartan and atenolol treatment.
The aim of our study was to investigate the effect of losartan on the changes in the early stages (at week 4) of experimental chronic renal failure after 5/6 nephrectomy compared with the impact of atenolol. Attention was focused on the ultrastructural changes in the renal corpuscles. Twenty-seven male Wistar rats were divided into three groups: nephrectomized group, nephrectomized losartan-treated group and nephrectomized atenolol-treated group. Rats were kept in a climate-controlled facility, where animals were housed under standard conditions on a 12-hour light/dark cycle and fed with standard rodent chow. Angiotensin receptor antagonist losartan (180 mg/L) or beta-blocking agent atenolol (750 mg/L) was added to the drinking water and treatment was started on the first day after the operation. Systolic blood pressure and 24 hour protein excretion was measured every week. Nephrectomized rats had higher proteinuria and systolic blood pressure than the treated rats. Rats were killed 4 weeks after surgery. Early stage renal disease was characterized by glomerular hypertrophy and focal segmental glomerulosclerosis. The morphological study revealed that ultrastructural changes in the atenolol-treated group were smaller than those in the nephrectomized and losartan-treated groups. Glomerular basement membrane (GBM) thickness was significantly increased in losartan-treated (206.8 nm) and atenolol-treated (198.8 nm) rats compared to nephrectomized (169.2 nm) rats. The podocytes demonstrated hypertrophy and foot process effacement, especially in nephrectomized group. In conclusion, our results show that firstly, treatment with losartan and atenolol significantly increased GBM thickening and secondly, treatment with atenolol reduced ultrastructural changes in the podocytes.
Aunapuu
Marina
M
Department of Anatomy, University of Tartu, Ravila 19, 51014 Tartu, Estonia. mariaun@ut.ee
Pechter
Ulle
U
Arend
Andres
A
Suuroja
Toivo
T
Ots
Mai
M
D000319:Adrenergic beta-Antagonists / Q000008:administration & dosage / Q000494:pharmacology*; D000804:Angiotensin II / Q000037:antagonists & inhibitors*; D057911:Angiotensin Receptor Antagonists; D000818:Animals; D001262:Atenolol / Q000008:administration & dosage / Q000494:pharmacology*; D001485:Basement Membrane / Q000187:drug effects; D004195:Disease Models, Animal; D005923:Glomerulosclerosis, Focal Segmental / Q000209:etiology / Q000473:pathology; D006984:Hypertrophy; D007676:Kidney Failure, Chronic / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D007678:Kidney Glomerulus / Q000166:cytology / Q000187:drug effects* / Q000473:pathology / Q000648:ultrastructure*; D019808:Losartan / Q000008:administration & dosage / Q000494:pharmacology*; D008297:Male; D008854:Microscopy, Electron; D009392:Nephrectomy; D011507:Proteinuria / Q000175:diagnosis / Q000209:etiology; D051381:Rats; D017208:Rats, Wistar; D013599:Systole; D013997:Time Factors
D000319:Adrenergic beta-Antagonists; D057911:Angiotensin Receptor Antagonists; D000804:Angiotensin II; D001262:Atenolol; D019808:Losartan