Tags

Type your tag names separated by a space and hit enter

Endothelial nitric oxide modulates perivascular sensory neurotransmission in the rat isolated mesenteric arterial bed.
Br J Pharmacol. 2002 Sep; 137(1):19-28.BJ

Abstract

1. A possible role of nitric oxide (NO) as a modulator of capsaicin-sensitive sensory neurotransmission in blood vessels was investigated in the rat isolated mesenteric arterial bed. 2. Electrical field stimulation (EFS) of methoxamine-preconstricted mesenteric beds elicited frequency-dependent vasorelaxation mediated by capsaicin-sensitive sensory nerves. N(G)-nitro-L-arginine methyl ester (L-NAME, 10 and 300 microM) and 7-nitroindazole (7-NI, 100 microM), inhibitors of nitric oxide synthase (NOS), augmented sensory neurogenic vasorelaxation. D-NAME (300 microM), 6-aminoindazole (100 microM) and N(omega)-propyl-L-arginine (50 nM), a selective inhibitor of neuronal NOS, were without effect. The effect of 10 microM L-NAME was reversed by L-arginine (1 mM), the substrate for NOS. 3. L-NAME (300 microM) and 7-NI (100 microM) had no significant effect on vasorelaxations to calcitonin gene-related peptide (CGRP), the principal motor neurotransmitter of capsaicin-sensitive sensory nerves in rat mesenteric arteries, or to capsaicin, indicating a prejunctional action. The inhibitors of NOS had no effect on vasorelaxation to forskolin, but augmented vasorelaxation to sodium nitroprusside (SNP). 4. Removal of the endothelium augmented sensory neurogenic vasorelaxation, but did not affect vasorelaxation to CGRP, indicating a prejunctional action of endothelial NO. 5. In the absence of endothelium, L-NAME (300 microM) inhibited, and 7-NI (100 microM) caused no further augmentation of sensory neurotransmission. 6. SNP (100 nM), a nitric oxide donor, attenuated sensory neurogenic relaxations to EFS. 7. In rat isolated thoracic aortic rings, L-NAME (100 microM) and 7-NI (100 microM) attenuated concentration-dependent relaxations to acetylcholine. 8. These data show that NO modulates sensory neurotransmission evoked by EFS of the rat isolated mesenteric arterial bed, and that when NO synthesis is blocked sensory neurogenic relaxation is augmented. The source of NO is the vascular endothelium.

Authors+Show Affiliations

School of Biomedical Sciences, University of Nottingham Medical School, Queen's Medical Centre, Nottingham NG7 2UH. vera.ralevic@nottingham.ac.uk

Pub Type(s)

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

Language

eng

PubMed ID

12183327

Citation

Ralevic, Vera. "Endothelial Nitric Oxide Modulates Perivascular Sensory Neurotransmission in the Rat Isolated Mesenteric Arterial Bed." British Journal of Pharmacology, vol. 137, no. 1, 2002, pp. 19-28.
Ralevic V. Endothelial nitric oxide modulates perivascular sensory neurotransmission in the rat isolated mesenteric arterial bed. Br J Pharmacol. 2002;137(1):19-28.
Ralevic, V. (2002). Endothelial nitric oxide modulates perivascular sensory neurotransmission in the rat isolated mesenteric arterial bed. British Journal of Pharmacology, 137(1), 19-28.
Ralevic V. Endothelial Nitric Oxide Modulates Perivascular Sensory Neurotransmission in the Rat Isolated Mesenteric Arterial Bed. Br J Pharmacol. 2002;137(1):19-28. PubMed PMID: 12183327.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Endothelial nitric oxide modulates perivascular sensory neurotransmission in the rat isolated mesenteric arterial bed. A1 - Ralevic,Vera, PY - 2002/8/17/pubmed PY - 2003/3/20/medline PY - 2002/8/17/entrez SP - 19 EP - 28 JF - British journal of pharmacology JO - Br J Pharmacol VL - 137 IS - 1 N2 - 1. A possible role of nitric oxide (NO) as a modulator of capsaicin-sensitive sensory neurotransmission in blood vessels was investigated in the rat isolated mesenteric arterial bed. 2. Electrical field stimulation (EFS) of methoxamine-preconstricted mesenteric beds elicited frequency-dependent vasorelaxation mediated by capsaicin-sensitive sensory nerves. N(G)-nitro-L-arginine methyl ester (L-NAME, 10 and 300 microM) and 7-nitroindazole (7-NI, 100 microM), inhibitors of nitric oxide synthase (NOS), augmented sensory neurogenic vasorelaxation. D-NAME (300 microM), 6-aminoindazole (100 microM) and N(omega)-propyl-L-arginine (50 nM), a selective inhibitor of neuronal NOS, were without effect. The effect of 10 microM L-NAME was reversed by L-arginine (1 mM), the substrate for NOS. 3. L-NAME (300 microM) and 7-NI (100 microM) had no significant effect on vasorelaxations to calcitonin gene-related peptide (CGRP), the principal motor neurotransmitter of capsaicin-sensitive sensory nerves in rat mesenteric arteries, or to capsaicin, indicating a prejunctional action. The inhibitors of NOS had no effect on vasorelaxation to forskolin, but augmented vasorelaxation to sodium nitroprusside (SNP). 4. Removal of the endothelium augmented sensory neurogenic vasorelaxation, but did not affect vasorelaxation to CGRP, indicating a prejunctional action of endothelial NO. 5. In the absence of endothelium, L-NAME (300 microM) inhibited, and 7-NI (100 microM) caused no further augmentation of sensory neurotransmission. 6. SNP (100 nM), a nitric oxide donor, attenuated sensory neurogenic relaxations to EFS. 7. In rat isolated thoracic aortic rings, L-NAME (100 microM) and 7-NI (100 microM) attenuated concentration-dependent relaxations to acetylcholine. 8. These data show that NO modulates sensory neurotransmission evoked by EFS of the rat isolated mesenteric arterial bed, and that when NO synthesis is blocked sensory neurogenic relaxation is augmented. The source of NO is the vascular endothelium. SN - 0007-1188 UR - https://www.unboundmedicine.com/medline/citation/12183327/Endothelial_nitric_oxide_modulates_perivascular_sensory_neurotransmission_in_the_rat_isolated_mesenteric_arterial_bed_ L2 - https://doi.org/10.1038/sj.bjp.0704837 DB - PRIME DP - Unbound Medicine ER -