• Pascual Medina, Gloria Segarra, Marta Peiro, Blas Flor, Juan B Martínez-León, José M Vila, and Salvador Lluch.
• Departamento de Fisiología, Facultad de Medicina y Odontología, Universidad de Valencia, Valencia, Spain. medinap@post.uv.es
• Am. J. Hypertens. 2003 Jan 1;16(1):28-32.

BackgroundThe objective of this study was to characterize the neurogenic contraction and relaxation of the human gastroepiploic artery and to determine whether the responses are mediated by nitric oxide (NO) from neural or endothelial origin.MethodsRings of human gastroepiploic artery were obtained from 18 patients (12 men, 6 women) undergoing gastrectomy. The rings were suspended in organ baths for isometric recording of tension. We studied the contractile and relaxant responses to electrical field stimulation.ResultsIn arteries under resting conditions, electrical field stimulation (2 to 8 Hz) caused frequency-dependent contractions that were of greater magnitude in arteries denuded of endothelium and blocked by tetrodotoxin (10(-6) mol/L). The inhibitor of NO synthesis N(G)-monomethyl-L-arginine (L-NMMA, 10(-4) mol/L) increased contractile responses only in arteries with endothelium. In preparations contracted with norepinephrine in the presence of guanethidine (10(-6) mol/L) and atropine (10(-6) mol/L), electrical stimulation induced frequency-dependent relaxations. This neurogenic relaxation was prevented by L-NMMA (10(-4) mol/L) and tetrodotoxin (10(-6) mol/L), but was unaffected by removal of the endothelium.ConclusionsThe results provide functional evidence that NO is released by autonomic nerves of the human gastroepiploic artery. We hypothesize that the release of NO from both endothelial and neurogenic origin may modulate resistance of the human gastroepiploic artery. Dysfunction in any of these sources of NO should be considered in some form of vasospasm.

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