Letter to the Editor |
Hôpital Lariboisière, INSERM Unit 541, Paris, France, matrougui9@hotmail.com
To the Editor:
The study of Sausbier et al,1 published in a recent issue of Circulation Research, investigated the mechanism of nitric oxide (NO)/cGMP-dependent vasorelaxation. For this purpose, the authors carried out a series of experiments using both large and small resistance arteries from wild-type and cGMP kinase I-deficient (cGKI-/-) mice. The experiments were performed using two different techniques, the wire-based isometric tension technique (wire myograph) and the pressure-perfusion technique (arteriograph). The aim of the present commentary is to point out some methodological issues that, we believe, should be taken into account when extrapolating results from large arteries onto small resistance arteries: (1) Differences in anatomic structure of large and resistance arteries.2 (2) Differences in the significance of contractile and relaxant function of large and resistance arteries. (3) Differences in the mechanisms of myogenic and agonist-induced precontractile responses and in the mediators of endothelium-dependent relaxation in large and resistance arteries. (4) Differences in the responsiveness of wire-mounted (isometric) and pressurized (isobaric) arterial preparations.
To study the relaxant responses, resistance arteries were precontracted by changing the intraluminal pressure (myogenic activation), whereas large arteries were precontracted by norepinephrine (
-adrenergic activation). The different activation also refers to the marked differences in the primary function of large and resistance arteries. Resistance arteries are indeed continuously subjected to changes in mechanical forces (flow and pressure) that regulate active vasomotion, fitting blood flow continuously to local demands. The primary function of large arteries is, however, different, and it is rather to damp the energy generated by
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