Estrogen administration has a number of favorable cardiovascular effects, a
nd recent evidence suggests that these include an increase in arterial dist
ensibility. Whether this is also the case for the physiological changes in
estrogen production during the menstrual cycle has never been determined, h
owever. In 21 premenopausal healthy women, we continuously measured radial
artery diameter and blood pressure by an echo-tracking device and a beat-to
-beat finger device, respectively. Arterial distensibility was calculated a
s distensibility/blood pressure curve. The measurements were made during th
e follicular, ovulatory, and luteal phases of the menstrual cycle. As expec
ted, compared with the follicular phase, plasma estradiol, follicle-stimula
ting hormone, luteinizing hormone, and prolactin were increased in the ovul
atory phase, whereas progesterone was increased in the luteal phase, togeth
er with antidiuretic hormone. Radial artery distensibility was increased in
the ovulatory and reduced in the luteal phase, the changes being independe
nt of the small, concomitant blood pressure changes. The arterial wall stif
fening seen in the luteal phase was associated with a reduction in the flow
-dependent endothelial dilatation of the radial artery as assessed by the h
yperemia after short-term ischemia of the hand. Thus, the natural menstrual
cycle is characterized by alterations in radial artery distensibility. The
mechanisms responsible for this phenomenon remain to be clarified. It is p
ossible, however, that the greater arterial distensibility of the ovulatory
phase is due to an estrogen-dependent reduction in vascular smooth muscle
tone, whereas the arterial stiffening of the luteal phase depends on vascul
ar smooth muscle contraction due to more complex hormonal phenomena, ie, an
endothelial impairment due to estrogen reduction but also to an increase i
n progesterone and antidiuretic hormone levels.