Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Learmont, J.G. et al.

Nitric oxide is involved in flow-induced dilation of isolated human small fetoplacental arteries.

OBJECTIVES: The aim of this study was to determine the dilation that occurs in response to increments of intraluminal flow in isolated human small fetoplacental arteries and to investigate the role played by nitric oxide. STUDY DESIGN: Small fetoplacental arteries (mean luminal diameter 482 +/- 31 micrometers, n = 17, at zero flow and pressure) were dissected from samples of placental tissue obtained from normal term vaginal deliveries and elective term cesarean sections for breech presentation. The arteries were mounted on a pressure myograph, and the response to increasing intraluminal flow was investigated in the presence and absence of a nitric oxide synthase inhibitor (N-omega-nitro-L-arginine methyl ester, 10(-4) mol/L). Basal tone was assessed in a separate group of arteries (n=7) by the removal of extracellular calcium. RESULTS: The presence of significant basal tone was demonstrated in these arteries. The arteries dilated in response to increasing luminal flow, and the dilation was significantly reduced by inhibition of nitric oxide synthase (control, 5.5% +/- 1.0% increase in artery diameter, n=10, vs 0.95 +/- 0.94, n=10, in the presence of N-omega-nitro-L-arginine methyl ester, 10(-4) mol/L, p<0.01). CONCLUSIONS: The data substantiate previous indirect studies suggesting that nitric oxide plays a role in the fetoplacental circulation. Flow-induced nitric oxide release in the stem villous arteries may make an important contribution to maintenance of this low-resistance circulation.[1]

References

Nitric oxide is involved in flow-induced dilation of isolated human small fetoplacental arteries. Learmont, J.G., Poston, L. Am. J. Obstet. Gynecol. (1996) [Pubmed]

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