Key result
Nitric oxide synthase inhibition with L-NAME impaired glomerular filtration rate and aggravated glomerular sclerosis in polycythemic rats, effects ameliorated by an angiotensin receptor blocker.
Why the study?
Does nitric oxide synthase inhibition affect renal function and histology in polycythemic rats?
Does nitric oxide synthase inhibition affect renal function and histology in polycythemic rats?
In polycythemic rats, enhanced nitric oxide production buffers glomerular damage, and the balance between nitric oxide and angiotensin II is important for maintaining renal function and structure.
Should not alter clinical practice; extends preclinical evidence that nitric oxide buffers glomerular injury in polycythemia.
Augmented endogenous nitric oxide (NO) production may ameliorate derangement of renal functions or glomerular damage in polycythemia. To investigate this possibility, we examined the effect of NO synthase inhibition with N omega-nitro-L-arginine methyl ester (L-NAME; 50 mg/dl in drinking water) on renal functions and histology in heminephrectomized Sprague-Dawley rats treated for 4 weeks with recombinant human erythropoietin (rh-EP; 500 IU/kg on alternate days). L-NAME elevated the blood pressure which was aggravated by concomitant rh-EP and was ameliorated by treatment with a nonpeptide angiotensin type 1 receptor blocker (CV116; 60 mg/kg in chow). The hematocrit level was prominently increased by rh-EP. The glomerular filtration rate was impaired by L-NAME alone, but was maintained by concomitant administration of rh-EP or CV116. Micropuncture experiments revealed that the glomerular capillary pressure was similarly elevated by L-NAME alone or in combination with rh-EP. L-NAME significantly, although not prominently, aggravated glomerular sclerosis observed with rh-EP alone, and concomitant CV116 ameliorated the glomerular damage. These results suggest that, in polycythemia, enhanced NO production buffers the glomerular damage, and the balance between NO and angiotensin II may play an important role in maintaining renal function and glomerular structure.
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Kawata et al. (1998) studied Polycythemia. N omega-nitro-L-arginine methyl ester (L-NAME) was evaluated on Renal functions and histology. Nitric oxide synthase inhibition with L-NAME impaired glomerular filtration rate and aggravated glomerular sclerosis in polycythemic rats, effects ameliorated by an angiotensin receptor blocker.
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