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Neuronal nitric-oxide synthase inhibition facilitates adrenergic neurotransmission in rat mesenteric resistance arteries.
J Pharmacol Exp Ther. 2006 Feb; 316(2):490-7.JP

Abstract

The effects of nonselective nitric-oxide synthase (NOS) inhibitors [N-omega-nitro-L-arginine methyl ester (L-NAME) and N-omega-nitro-L-arginine (L-NNA)] and specific neuronal NOS (nNOS) inhibitor [vinyl-L-N-5-(1-imino-3-butenyl)-L-ornithine (L-VNIO)] on adrenergic nerve-mediated vasoconstriction were studied in rat perfused mesenteric vascular beds without endothelium. Perfusion of L-NAME, L-NNA, or l-VNIO markedly augmented vasoconstrictor responses to periarterial nerve stimulation (PNS; 2-8 Hz) without affecting vasoconstriction induced by exogenously injected norepinephrine (NE). Addition of L-arginine, a precursor for the synthesis of nitric oxide (NO), reversed the augmentation of the PNS response by l-NAME. The PNS (8 Hz)-evoked NE release in the perfusate was increased by L-NAME perfusion. In preparations treated with capsaicin [a depleter of calcitonin gene-related peptide (CGRP)-containing nerves], L-NAME did not augment vasoconstrictor responses to PNS or NE injection. Combined perfusion of CGRP(8-37) (a CGRP receptor antagonist) and L-NAME induced additive augmentation of the vasoconstrictor response to PNS but did not affect the response to NE injection. In preparations with active tone produced by methoxamine and in the presence of guanethidine, L-NAME perfusion did not affect the vasodilator response induced by PNS. Immunostaining of the mesenteric artery showed the presence of nNOS-like immunopositive nerve fibers, which were absent in arteries pretreated with capsaicin. These findings suggest that NO, which is released from perivascular capsaicin-sensitive nerves, presynaptically inhibits neurogenic NE release to modulate adrenergic neurotransmission.

Authors+Show Affiliations

Department of Clinical Pharmaceutical Science, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16236814

Citation

Hatanaka, Yukako, et al. "Neuronal Nitric-oxide Synthase Inhibition Facilitates Adrenergic Neurotransmission in Rat Mesenteric Resistance Arteries." The Journal of Pharmacology and Experimental Therapeutics, vol. 316, no. 2, 2006, pp. 490-7.
Hatanaka Y, Hobara N, Honghua J, et al. Neuronal nitric-oxide synthase inhibition facilitates adrenergic neurotransmission in rat mesenteric resistance arteries. J Pharmacol Exp Ther. 2006;316(2):490-7.
Hatanaka, Y., Hobara, N., Honghua, J., Akiyama, S., Nawa, H., Kobayashi, Y., Takayama, F., Gomita, Y., & Kawasaki, H. (2006). Neuronal nitric-oxide synthase inhibition facilitates adrenergic neurotransmission in rat mesenteric resistance arteries. The Journal of Pharmacology and Experimental Therapeutics, 316(2), 490-7.
Hatanaka Y, et al. Neuronal Nitric-oxide Synthase Inhibition Facilitates Adrenergic Neurotransmission in Rat Mesenteric Resistance Arteries. J Pharmacol Exp Ther. 2006;316(2):490-7. PubMed PMID: 16236814.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Neuronal nitric-oxide synthase inhibition facilitates adrenergic neurotransmission in rat mesenteric resistance arteries. AU - Hatanaka,Yukako, AU - Hobara,Narumi, AU - Honghua,Jin, AU - Akiyama,Shinji, AU - Nawa,Hideki, AU - Kobayashi,Yuta, AU - Takayama,Fusako, AU - Gomita,Yutaka, AU - Kawasaki,Hiromu, Y1 - 2005/10/19/ PY - 2005/10/21/pubmed PY - 2006/4/6/medline PY - 2005/10/21/entrez SP - 490 EP - 7 JF - The Journal of pharmacology and experimental therapeutics JO - J Pharmacol Exp Ther VL - 316 IS - 2 N2 - The effects of nonselective nitric-oxide synthase (NOS) inhibitors [N-omega-nitro-L-arginine methyl ester (L-NAME) and N-omega-nitro-L-arginine (L-NNA)] and specific neuronal NOS (nNOS) inhibitor [vinyl-L-N-5-(1-imino-3-butenyl)-L-ornithine (L-VNIO)] on adrenergic nerve-mediated vasoconstriction were studied in rat perfused mesenteric vascular beds without endothelium. Perfusion of L-NAME, L-NNA, or l-VNIO markedly augmented vasoconstrictor responses to periarterial nerve stimulation (PNS; 2-8 Hz) without affecting vasoconstriction induced by exogenously injected norepinephrine (NE). Addition of L-arginine, a precursor for the synthesis of nitric oxide (NO), reversed the augmentation of the PNS response by l-NAME. The PNS (8 Hz)-evoked NE release in the perfusate was increased by L-NAME perfusion. In preparations treated with capsaicin [a depleter of calcitonin gene-related peptide (CGRP)-containing nerves], L-NAME did not augment vasoconstrictor responses to PNS or NE injection. Combined perfusion of CGRP(8-37) (a CGRP receptor antagonist) and L-NAME induced additive augmentation of the vasoconstrictor response to PNS but did not affect the response to NE injection. In preparations with active tone produced by methoxamine and in the presence of guanethidine, L-NAME perfusion did not affect the vasodilator response induced by PNS. Immunostaining of the mesenteric artery showed the presence of nNOS-like immunopositive nerve fibers, which were absent in arteries pretreated with capsaicin. These findings suggest that NO, which is released from perivascular capsaicin-sensitive nerves, presynaptically inhibits neurogenic NE release to modulate adrenergic neurotransmission. SN - 0022-3565 UR - https://www.unboundmedicine.com/medline/citation/16236814/Neuronal_nitric_oxide_synthase_inhibition_facilitates_adrenergic_neurotransmission_in_rat_mesenteric_resistance_arteries_ L2 - https://jpet.aspetjournals.org/cgi/pmidlookup?view=long&pmid=16236814 DB - PRIME DP - Unbound Medicine ER -