Endothelium determines stabilization of the pressure drop in arteries

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Abstract
To ascertain whether the relative invariance of the pressure drop along the arterial cascade--from the aortic arch down to include the saphenous artery--during increases of saphenous outflow (Khayutin et al. 1993), is determined mainly by dilation of the latter, and to discover whether this invariability is a manifestation of endothelium-mediated vasodilation, the pressure drop along the rat saphenous artery was measured in situ during exposure of the artery to rectangular pulses or slow ramps of blood flow. At flow rates below a critical value of about 0.3 ml min-1, flow increase was followed by a proportional increase of pressure drop. In contrast, with further flow increase, up to the values five to six times beyond the critical one, the steady state pressure drop did not increase at all, or only to a minor extent. This 'pressure drop stabilization' was shown to be unrelated to the decline of distending pressure, but to result from a true artery dilation commensurate with the flow increase. Interference with the endothelium by way of 90 mM hydrogen peroxide eliminated the stabilization effect, whereas noradrenaline-induced constrictions could be increased about three-fold. The 'threshold' shear stress on the endothelium, needed to initiate saphenous artery dilation, was estimated to be 74 +/- 4 dyn cm-2. The functional importance of stabilizing the pressure drop along the arterial conductance and resistance vessels is discussed.