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The present study was undertaken to examine the influence of transmural pressure on vasomotion and to determine if any such influence was endothelium-dependent. Responses to changes in intravascular pressure of cannulated mesenteric small arteries were investigated under no-flow conditions. Both intact and endothelium-denuded arteries dilated passively when intravascular pressure was increased stepwise from 20 to 140 mmHg. When tone was induced by noradrenaline, pressure increase resulted only in dilatation, independent of endothelium. The sensitivity to noradrenaline was significantly increased in vessels without endothelium, indicating a relaxing influence of the endothelium. Rhythmic contractions in response to noradrenaline occurred in all intact arteries, but were absent when the endothelium was removed. The amplitude of the rhythmic contractions decreased significantly when transmural pressure was elevated. The frequency increased when pressure was elevated from 20 to 80 mmHg and then remained rather constant during further pressure increases. As shown previously in non-pressurized arteries, exogenous cyclic GMP induced oscillations in endothelium-denuded arteries. Pressure-related effects on vasomotion were not dependent on an intact endothelium. Ryanodine, ouabain or verapamil inhibited the rhythmic activity, confirming previous results in non-pressurized arteries. Thus, changes in transmural pressure can modulate vasomotion, but this effect does not appear to be mediated by the endothelium. Generation of vasomotion may depend on release of Ca2+ from intracellular stores, the activity of the Na+, K(+)-pump and transmembrane Ca2+ inflow in a pressurized artery as shown previously in these arteries under isometric conditions.

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