Interactions of hormonal status and smoking on cardiovascular reactivity to laboratory stress in women

University of York (2002) J Physiol 539P, S131

Communications: Interactions of hormonal status and smoking on cardiovascular reactivity to laboratory stress in women

E. Tansey and C. Bell

Department of Physiology, Trinity College, Dublin 2, Ireland

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In young men, cigarette smoking reduces endothelium-mediated vasodilatation and increases cardiovascular sympathetic reactivity. Some recent data on these effects are reported at this meeting (Barry & Bell, 2001; Morris & Bell, 2001). Since the incidence of cardiovascular disease is lower in premenopausal women than in men or after menopause, due at least in part to the protective action of oestrogen (Mendelsohn & Karas, 1999), we were interested to determine whether cardiovascular behaviour in young women is subject to hormonal variation and is affected similarly to that of young men by smoking.

Female non-smokers (n = 9; age 23 ± 3 years, mean ± S.D.) and smokers (n = 6; age 23 ± 1 years; cigarette consumption 17 ± 4 day-1) were recruited with institutional ethics approval. All had regular menstrual cycles and all were tested both during menstruation (M) and at ovulation (O) as assessed by urinary LH. We monitored blood pressure and heart rate by applanation tonometry, stroke volume by impedance cardiography and forearm blood flow by venous occlusion plethysmography, at rest and during isometric handgrip, mental arithmetic and forearm reactive hyperaemia following 3 min arterial occlusion. A two-tailed Student’s t test was used in statistical analysis.

Resting mean arterial pressure was higher at O than at M and was higher at both phases of the cycle in smokers than in non-smokers (M: 76 ± 2 cf. 63 ± 2 mmHg; O: 85 ± 3 cf. 76 ± 2 mmHg, mean ± S.E.M.). No significant group differences in resting values of other parameters were seen. Handgrip increased blood pressure, heart rate and total peripheral resistance but, by contrast with the situation in men (Morris & Bell, 2001), mental arithmetic increased only heart rate. Neither hormonal nor smoking status affected these sympathetic stressor responses. Similarly, there were no differences in the magnitudes of reactive hyperaemic responses between M and O or between smokers and non-smokers (M: 13 ± 3 cf. 11 ± 2 ml min-1 100 ml-1, O: 10 ± 1 cf. 11 ± 3 ml min-1 100 ml-1).

In summary, resting blood pressure in young women varies with hormonal profile and, as in young men, it is elevated by moderate cigarette consumption. Sympathetic cardiovascular responses to standardised stressors are less marked in females than in males. Furthermore, while smoking exaggerates these sympathetic responses and attenuates forearm reactive hyperaemia, in men (Barry & Bell, 2001; Morris & Bell, 2001), neither type of resonse is so affected by smoking in women.

We thank Carter-Wallace Ltd for the generous donation of First Response Ovulation Kits.




Where applicable, experiments conform with Society ethical requirements.

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