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Am J Physiol Regul Integr Comp Physiol (January 17, 2002). doi:10.1152/ajpregu.00697.2001
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Articles in PresS, published online ahead of print January 17, 2002
Am J Physiol Regu Physiol, 10.1152/ajpregu.00697.2001
Submitted on November 21, 2001
Accepted on December 27, 2001

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

Hideki Tanioka1, Koichi Nakamura1, Shinsei Fujimura1, Makoto Yoshida1, Mizue Suzuki-Kusaba1, Hiroaki Hisa1*, and Susumu Satoh1

1 Department of Laboratory of Pharmacology, Tohoku University Graduate School of Pharmaceutical Sciences, Sendai, Miyagi, Japan

* To whom correspondence should be addressed. E-mail: hhisa{at}mail.pharm.tohoku.ac.jp.

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. Non-selective NOS inhibitors N{omega}-nitro-L-arginine methyl ester or N{omega}-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 N{omega}-nitro-L-arginine methyl ester on the RNS-induced responses. Carboxy-PTIO that eliminates NO by oxidizing to NO2 suppressed the NE efflux response whereas the perfusion pressure response was less susceptible to carboxy-PTIO. 8-Br-cGMP suppressed and a guanylate cyclase inhibitor NS2028 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 NO synthase does not contribute to these modulatory mechanisms in the sympathetic nervous system of the rat kidney.




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