The combined effects of defined changes in ventilation and stress-induced vasoconstriction were studied in the intestinal vascular bed in cats (n = 20) anaesthetized with fentanyl, nitrous oxide and diazepam. Intestinal reflex vasoconstriction was induced by stimulation either of the hypothalamic defence-alarm area or of somatic and visceral pain afferents. The volume-controlled ventilation was changed by altering the tidal volume, and stimulations were performed during either control conditions (Paco2 4.5-5.0 kPa), hyperventilation (Paco2 3.0-3.5 kPa) or hypoventilation (Paco2 6.5-7.5 kPa). The increase in intestinal vascular resistance (IVR) elicited by defence-alarm area stimulation was potentiated during hyperventilation (306 +/- 83% vs 198 +/- 62%; P less than 0.01) and attenuated during hypoventilation (176 +/- 62% vs 240 +/- 44%; P less than 0.05). The increase in IVR elicited by pain fibre stimulation was potentiated during hyperventilation (73 +/- 21% vs 54 +/- 19%; P less than 0.01), but not significantly changed during hypoventilation (47 +/- 19% vs 68 +/- 34% during control ventilation). Our data indicate that the ventilatory pattern can be decisive for the vasoconstrictor response during experimental stress. We suggest that remote neurogenic mechanisms account for the increased responsiveness during hyperventilation. The decreased responsiveness during hypoventilation, on the other hand, seems to correlate with the local vasodilator effects of carbon dioxide.