Invited Symposium: Hypertension III: Flow-Induced Vascular Remodeling



Materials & Methods


Discussion & Conclusion



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Ceiler, D (Dept. of Pharmacology, Universiteit Maastricht, The Netherlands)
De Mey, JGR (Dept. of Pharmacology, Universiteit Maastricht, The Netherlands)

Contact Person: Debbie Ceiler (D.Ceiler@Farmaco.unimaas.nl)


Increases in arterial blood flow lead to vasodilatation in muscular arteries and resistance arteries/arterioles, including arcading arterioles that are candidate collateral channels in ischemia. Nitric oxide (NO) is involved in the acute flow-induced vasodilator response. We addressed the chronic role of NO in flow-induced responses. In 8 week old male Wistar Kyoto rats, changes in blood flow (BF) were induced in small mesenteric muscular arteries by ligating every other first order mesenteric side branch in part of the mesenteric vascular bed, hereby reducing BF in ligated vessels (LO) and increasing BF in the intermediate parallel vessels (HI). Four LO and 3 HI were created near either the stomach or the coecum. This model is an adaptation of our earlier ligation model (Am.J.Physiol. 273: H1699-H1709) since vessels from the distant unoperated part of the vascular bed could be used as internal controls (CON). BF was measured with a Transonic flow probe in HI, LO and CON within 30 min. after ligation (t0; n=9). After surgery, rats received either no treatment (NT; n=10) or chornic administration of measured in mesenteric arteries of unoperated 10 week old male rats (sham; n=6)). No differences in flow were observed between CON (0.210.02 ml/min) or sham (0.260.04). Ligation of NT arteries reduced flow at t0 (0.030.02) in LO, which remained low at t2 (0.040.01). HI arteries of NT rats had a slightly increased flow at t0 (0.450.05) which became (0.170.03) or LO (0.030.01), but prevented the increase of BF in HI (0.270.05). Thus, although NO synthase inhibition did not compromise perfusion of the intact mesenteric circulation, it persistently prevented the fall in resistance offerred by arcading collateral arterioles. We speculate that the 'endothelium dysfunction' observed in hypertension, diabetes, and hyperlipidemia may impede the formation of adequate collateral circulations

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Presentation Number SAceiler0841
Keywords: remodelling, NO, rat

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Ceiler, D; De Mey, JGR; (1998). . Presented at INABIS '98 - 5th Internet World Congress on Biomedical Sciences at McMaster University, Canada, Dec 7-16th. Invited Symposium. Available at URL http://www.mcmaster.ca/inabis98/prewitt/ceiler0841/index.html
© 1998 Author(s) Hold Copyright