title: Fluctuations of radial artery distensibility throughout the menstrual cycle.
abstract: Estrogen administration has a number of favorable cardiovascular effects, and recent evidence suggests that these include an increase in arterial distensibility. Whether this is also the case for the physiological changes in estrogen production during the menstrual cycle has never been determined, however. 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 as distensibility/blood pressure curve. The measurements were made during the follicular, ovulatory, and luteal phases of the menstrual cycle. As expected, compared with the follicular phase, plasma estradiol, follicle-stimulating hormone, luteinizing hormone, and prolactin were increased in the ovulatory phase, whereas progesterone was increased in the luteal phase, together with antidiuretic hormone. Radial artery distensibility was increased in the ovulatory and reduced in the luteal phase, the changes being independent of the small, concomitant blood pressure changes. The arterial wall stiffening seen in the luteal phase was associated with a reduction in the flow-dependent endothelial dilatation of the radial artery as assessed by the hyperemia 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 possible, 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 vascular smooth muscle contraction due to more complex hormonal phenomena, ie, an endothelial impairment due to estrogen reduction but also to an increase in progesterone and antidiuretic hormone levels.
authors.affiliation: Cattedra di Medicina Interna I, Università degli Studi di Milano, Ospedale S. Gerardo, Monza, Centro di Fisiologia Clinica e Ipertensione, IRCSS, Ospedale Maggiore, Milan , Italy.
authors.forename: C
authors.initials: C
authors.lastname: Giannattasio
authors.forename: M
authors.initials: M
authors.lastname: Failla
authors.forename: A
authors.initials: A
authors.lastname: Grappiolo
authors.forename: M L
authors.initials: ML
authors.lastname: Stella
authors.forename: A
authors.initials: A
authors.lastname: Del Bo
authors.forename: M
authors.initials: M
authors.lastname: Colombo
authors.forename: G
authors.initials: G
authors.lastname: Mancia
mesh_terms: D000328:Adult; D004958:Estradiol / Q000097:blood; D005260:Female; D005640:Follicle Stimulating Hormone / Q000097:blood; D006801:Humans; D008183:Luteal Phase; D007986:Luteinizing Hormone / Q000097:blood; D008597:Menstrual Cycle; D009131:Muscle, Smooth, Vascular / Q000737:chemistry / Q000166:cytology; D010060:Ovulation / Q000502:physiology; D011388:Prolactin / Q000097:blood; D017534:Radial Artery / Q000033:anatomy & histology / Q000502:physiology*; D011960:Receptors, Estrogen / Q000378:metabolism; D014664:Vasodilation / Q000502:physiology
chemical_list: D011960:Receptors, Estrogen; D004958:Estradiol; D011388:Prolactin; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone