Send to

Choose Destination
See comment in PubMed Commons below
Psychosom Med. 1998 Mar-Apr;60(2):219-26.

Cardiovascular, endocrine, and receptor measures as related to sex and menstrual cycle phase.

Author information

  • 1Department of General and Comparative Physiology, University of Vienna, Austria.



The present study was undertaken to elucidate possible mechanisms underlying sex differences in cardiovascular measures or reactivity to challenge. Because there is vastly diverging literature on the issue, we tried to control for endocrine and psychological factors, which might contribute to some of the apparent discrepancies.


Blood pressure, heart rate, adrenaline, and noradrenaline in women (N = 24) and men (N = 14) were examined during baseline and challenge (Stroop Test and Cold Face Test). Adrenoceptor density on lymphocytes (beta 2) and platelets (alpha 2) were determined to examine possible sex differences in underlying cardiovascular mechanisms. Gender effects were controlled by assessing gender role orientation and task appraisal. Women were tested during either the follicular (N = 12) or the luteal (N = 12) phase of the menstrual cycle (verified by estradiol, progesterone, and luteinizing hormone).


Follicular and luteal phase women did not differ in any parameter except progesterone. We observed sex-related differences in absolute levels of physiological parameters, the male group having higher systolic blood pressure levels, higher adrenaline plasma concentrations, and significantly more alpha 2-adrenergic receptors. Both challenges elicited pronounced cardiovascular and endocrine responses. Men and women did not differ in response magnitude, in task appraisal, or gender role orientation.


The assumption that female sex hormones reduce reactivity to challenge is not supported by our data. The frequently reported male/female differences in reactivity may be caused by an interaction of gender and task characteristics.

[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Lippincott Williams & Wilkins
    Loading ...
    Write to the Help Desk