ISSN:
1432-2013
Keywords:
mRNA NO synthase inhibition NO synthase knockout Renin Renin content
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Abstract. Our study aimed to assess the roles of nitric oxide derived from endothelium NO-synthase (eNOS) and macula densa neuronal NO-synthase (nNOS) in the regulation of renal renin expression. For this purpose renin mRNA levels and renin content were determined in kidneys of wild-type (wt), nNOS-deficient (nNOS–/–), and eNOS-deficient (eNOS–/–) mice, in which the renin system was suppressed by feeding a high-salt diet (NaCl 4%), or was stimulated by feeding a low-salt (NaCl 0.02%) diet together with the converting-enzyme inhibitor ramipril (10 mg kg–1 day–1). In all mouse strains, renin mRNA levels were inversely related to the rate of sodium intake. In eNOS–/– mice renin mRNA levels and renal renin content were 50% lower than in wt mice at each level of salt intake, whilst in nNOS–/– mice renin expression was not different from wt controls. Administration of the general NO-synthase inhibitor nitro-l-arginine methyl ester (l-NAME, 50 mg kg–1 day–1) to mice kept on the low-salt/ramipril regimen caused a decrease of renal renin mRNA levels in wt and nNOS–/– mice, but not in eNOS–/– mice. These observations suggest that neither eNOS nor nNOS is essential for up- or downregulation of renin expression. eNOS-derived NO appears to enhance renin expression, whereas nNOS-derived NO does not.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/s004249900214
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