Original article
English
Wisam Elbishti
Department of Pharmacology, Faculty of Medicine, Al-Fateh University. Tripoli-Libya
JMJ Vol. 5, No 2 (Summer) 2006: 144-146
Abstract
Nitric oxide (NO) has been shown to alter kidney function by exerting diuretic and natriuretic effects. NO has also been shown to modulate central and peripheral sympathetic activity. Therefore, in order to investigate the possible role of renal sympathetic nerves in the renal effects of NO, the effects of the NO donor sodium nitroprusside ( SNP ) or the nitric oxide synthetase ( NOS ) inhibitor N-nitro-L-arginine methyl ester ( L-NAME ) on urine flow and urinary sodium excretion were studied in sham kidney-denervated and bilaterally kidney-denervated water-loaded ethanol-anaesthetized rats. In sham kidney-denervated rats, SNP produced diuretic and natriuretic effects, whereas L-NAME caused antidiuresis and antinatriuresis. In kidney-denervated rats, SNP and L-NAME did not cause any significant change in either urine flow or urinary sodium excretion. These results indicate that the renal effects of NO are mediated through inhibition of renal sympathetic nerves activity and therefore has important role in regulating the neural component of renal function.
Keywords: Nitric oxide, Renal function, Renal sympathetic nerves, Kidney-denervation
Link/DOI: http://www.jmj.org.ly/modules.php?name=News&file=article&sid=1140