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Am J Physiol Heart Circ Physiol 277: H1027-H1035, 1999;
0363-6135/99 $5.00
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Vol. 277, Issue 3, H1027-H1035, September 1999

Rise in endothelium-derived NO after stimulation of rat perivascular sympathetic mesenteric nerves

Mauricio P. Boric, Xavier F. Figueroa, M. Verónica Donoso, Alfonso Paredes, Inés Poblete, and J. Pablo Huidobro-Toro

Unidad de Regulación Neurohumoral, Departamento de Ciencias Fisiológicas, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Santiago, Chile

To evaluate whether sympathetic activity induces nitric oxide (NO) production, we perfused the rat arterial mesenteric bed and measured luminally accessible norepinephrine (NE), NO, and cGMP before, during, and after stimulation of perivascular nerves. Electrical stimulation (1 min, 30 Hz) raised perfusion pressure by 97 ± 7 mmHg, accompanied by peaks of 23 ± 3 pmol NE, 445 ± 48 pmol NO, and 1 pmol cGMP. Likewise, perfusion with 10 µM NE induced vasoconstriction coupled to increased NO and cGMP release. Electrically elicited NO release depended on stimulus frequency and duration. Endothelium denudation with saponin abolished the NO peak without changing NE release. Inhibition of NO synthase with 100 µM Nomega -nitro-L-arginine reduced basal NO and cGMP release and blocked the electrically stimulated and exogenous NE-stimulated NO peak while enhancing vasoconstriction. Blocking either sympathetic exocytosis with 1 µM guanethidine or alpha 1-adrenoceptors with 30 nM prazosin abolished the electrically evoked vasoconstriction and NO release. alpha 2-Adrenoceptor blockade with 1 µM yohimbine reduced both vasoconstriction and NO peak while increasing NE release. In summary, sympathetically released NE induces vasoconstriction, which triggers a secondary release of endothelial NO coupled to cGMP production.

nitric oxide chemiluminescence; norepinephrine; guanosine 3',5'-cyclic monophosphate release; sympathetic neurotransmission; rat arterial mesenteric bed; endothelial activation; adrenoceptor blockade


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