Venoconstriction is one of the compensatory adjustments during orthostasis to counter venous pooling. The female hormones oestrogen and progesterone are known for their relaxant effects on arterial vessels and both can cause venodilation (Nekooeian & Pang, 2000; Herket et al. 2000). By contrast, oestrogen has been reported to enhance venoconstriction to noradrenaline (Varbiro et al. 2002). It is not clear, therefore, how venoconstriction is modulated during the normal menstrual cycle or by the action of exogenous hormones (oral contraceptive). To investigate this, we compared calf volume (strain gauge plethysmography) during sympathoexcitation to induce venoconstriction in 6 female subjects with normal menstrual cycles (N), age 21 ± 2 yrs, body mass index 24 ± 5 (both mean ± SD), and 7 females taking the combined oral contraceptive (O), age 20 ± 1 yrs, body mass index 21 ± 2. With subjects supine, venous distension was induced 3 times in the left leg by cuff inflation (50 mmHg for 6 mins), one control (CON) and two with the interventions of either contralateral isometric leg exercise (ILE, 40 % maximum voluntary plantarflexion force) or mental stress test (MST, mental arithmetic) applied between mins 3-5. Changes in calf volume during interventions were compared with those during CON distension, such that a decrease in volume would indicate venoconstriction (Zelis & Mason, 1969). All women were tested on two occasion, once during the menstrual phase (M) of their cycle (days 1-5) and again during the luteal (L) phase (days 21-28). Mean arterial blood pressures and heart rates (Portapres, right hand) did not differ between cycle phases in either group (N M 93 ± 7 mmHg, 60 ±3 bpm.; N L 88 ± 4 mmHg, 70 ± 5 bpm; O M 85 ±5 mmHg, 64 ±3 bpm.; OC L 85 ± 3 mmHg, 65 ± 3 bpm). Sympathoexcitation was confirmed by increases in blood pressure and heart rate which were similar in N women in both cycle phases for the ILE intervention (M 4 ± 1 mmHg, 9 ± 3 bpm; L 5 ± 2 mmHg, 10 ± 5 bpm) and MST (M 9 ± 3 mmHg, 14 ± 8 bpm; L 9 ± 2 mmHg, 7 ± 3 bpm). Likewise, O women showed increases in M of 8 ± 4 mmHg and 18 ± 5 bpm to ILE and 6 ± 3 mmHg and 9 ± 4 bpm to MST. Values in L were 7 ± 4 mmHg, 14 ± 5 bpm for ILE and 7 ± 2 mmHg and 13 ± 4 bpm for MST (NS between phases). In response to ILE, there was no significant change in calf volume in any women in either phase. In response to MST, N women did not venoconstrict in either phase whereas O women tended to dilate in both phases. The lack of venoconstriction to sympathoexcitation by ILE is different from men, in whom a significant decrease in calf volume was observed previously (Brown et al. 2007). This could contribute to the orthostatic intolerance of women compared with men.