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Am J Physiol Regul Integr Comp Physiol 282: R1436-R1442, 2002. First published January 17, 2002; doi:10.1152/ajpregu.00697.2001
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Vol. 282, Issue 5, R1436-R1442, May 2002

Facilitatory role of NO in neural norepinephrine release in the rat kidney

Hideki Tanioka, Koichi Nakamura, Shinsei Fujimura, Makoto Yoshida, Mizue Suzuki-Kusaba, Hiroaki Hisa, and Susumu Satoh

Laboratory of Pharmacology, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai 980-8578, Japan

We examined modulation by nitric oxide (NO) of sympathetic neurotransmitter release and vasoconstriction in the isolated pump-perfused rat kidney. Electrical renal nerve stimulation (RNS; 1 and 2 Hz) increased renal perfusion pressure and renal norepinephrine (NE) efflux. Nonselective NO synthase (NOS) inhibitors [Nomega -nitro-L-arginine methyl ester (L-NAME) or Nomega -nitro-L-arginine], but not a selective neuronal NO synthase inhibitor (7-nitroindazole sodium salt), suppressed the NE efflux response and enhanced the perfusion pressure response. Pretreatment with L-arginine prevented the effects of L-NAME on the RNS-induced responses. 2-(4-Carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (carboxy-PTIO), which eliminates NO by oxidizing it to NO2, suppressed the NE efflux response, whereas the perfusion pressure response was less susceptible to carboxy-PTIO. 8-Bromoguanosine cGMP suppressed and a guanylate cyclase inhibitor [4H-8-bromo-1,2,4-oxadiazolo(3,4-d)benz(b)(1,4)oxazin-1-one] enhanced the RNS-induced perfusion pressure response, but neither of these drugs affected the NE efflux response. These results suggest that endogenous NO facilitates the NE release through cGMP-independent mechanisms, NO metabolites formed after NO2 rather than NO itself counteract the vasoconstriction, and neuronal NOS does not contribute to these modulatory mechanisms in the sympathetic nervous system of the rat kidney.

sympathetic nerves; vasoconstriction; nitric oxide synthase inhibitor; guanylate cyclase inhibitor; nitric oxide scavenger


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