Estrogen Attenuates the Pressor Response Mediated by the Group III Mechanoreflex.
10.4040/jkan.2011.41.2.191
- Author:
Seung Ae PARK
1
;
Jong Kyung KIM
Author Information
1. Graduate School of Physical Education, Kyung Hee University, Yongin, Korea. kyung19692002@khu.ac.kr
- Publication Type:Original Article ; Controlled Clinical Trial ; English Abstract
- Keywords:
Estrogen;
Post-menopausal woman;
Exercise pressor reflex;
Group III mechanoreceptors;
Cardiac output
- MeSH:
Aged;
Blood Pressure;
Body Mass Index;
Cardiac Output;
Estrogens/*metabolism;
Female;
Heart Rate;
Humans;
Mechanoreceptors;
Middle Aged;
Postmenopause;
Premenopause;
Reflex, Stretch/*physiology;
Stroke Volume
- From:Journal of Korean Academy of Nursing
2011;41(2):191-196
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: We investigated the effects of group III mechanoreceptors to cardiovascular responses in both pre-menopausal woman and post-menopausal woman during passive ankle dorsiflexion (PAD). METHODS: Twenty healthy volunteers (10 post-menopausal women and 10 pre-menopausal women) were recruited for this study. Stroke volume (SV), heart rate (HR), cardiac output (CO), and total vascular conductances (TVC) were measured continuously throughout the experiment. To stimulate the group III mechanoreceptors, PAD was performed for one minute. RESULTS: The results showed that mean arterial pressure (MAP) mediated by the mechanoreflex activation was significantly increased in both groups. However, this pressor response was significantly higher in post-menopausal women. This reflex significantly increased both SV and CO in pre-menopausal women, while there were no differences in post-menopausal women. There was no difference in HR in either group. The mechanoreflex significantly decreased TVC in post-menopausal woman, while there was no difference in pre-menopausal woman. CONCLUSION: The results indicate that the excessive pressor response mediated by the mechanoreflex occurs due to overactivity of group III mechanorecptors and the mechanism is produced mainly via peripheral vasoconstriction in post-menopausal women.
