title: Systemic and renal hemodynamic changes in the luteal phase of the menstrual cycle mimic early pregnancy.
abstract: Blood pressure decreases during early pregnancy in association with a decrease in peripheral vascular resistance and increases in renal plasma flow and glomerular filtration rate. These early changes suggest a potential association with corpora lutea function. To determine whether peripheral vasodilation occurs following ovulation, we studied 16 healthy women in the midfollicular and midluteal phases of the menstrual cycle. A significant decrease in mean arterial pressure in the midluteal phase of the cycle (midfollicular of 81.7 +/- 2.0 vs. midluteal of 75.4 +/- 2.3 mmHg, P < 0.005) was found in association with a decrease in systemic vascular resistance and an increase in cardiac output. Renal plasma flow and glomerular filtration rate increased. Plasma renin activity and aldosterone concentration increased significantly in the luteal phase accompanied by a decrease in atrial natriuretic peptide concentration. Serum sodium, chloride, and bicarbonate concentrations and osmolarity also declined significantly in the midluteal phase of the menstrual cycle. Urinary adenosine 3',5'-cyclic monophosphate (cAMP) excretion increased in the luteal compared with the follicular phase, whereas no changes in urinary cGMP or NO2/NO3 excretion were found. Thus peripheral vasodilation occurs in the luteal phase of the normal menstrual cycle in association with an increase in renal plasma flow and filtration. Activation of the renin-angiotensin-aldosterone axis is found in the luteal phase of the menstrual cycle. These changes are accompanied by an increase in urinary cAMP excretion indicating potential vasodilating mediators responsible for the observed hemodynamic changes.
authors.affiliation: University of Colorado Health Sciences Center, Denver 80262, USA.
authors.forename: A B
authors.initials: AB
authors.lastname: Chapman
authors.forename: S
authors.initials: S
authors.lastname: Zamudio
authors.forename: W
authors.initials: W
authors.lastname: Woodmansee
authors.forename: A
authors.initials: A
authors.lastname: Merouani
authors.forename: F
authors.initials: F
authors.lastname: Osorio
authors.forename: A
authors.initials: A
authors.lastname: Johnson
authors.forename: L G
authors.initials: LG
authors.lastname: Moore
authors.forename: T
authors.initials: T
authors.lastname: Dahms
authors.forename: C
authors.initials: C
authors.lastname: Coffin
authors.forename: W T
authors.initials: WT
authors.lastname: Abraham
authors.forename: R W
authors.initials: RW
authors.lastname: Schrier
mesh_terms: D000328:Adult; D000450:Aldosterone / Q000378:metabolism; D009320:Atrial Natriuretic Factor / Q000378:metabolism; D001639:Bicarbonates / Q000097:blood; D001794:Blood Pressure; D001810:Blood Volume; D002302:Cardiac Output; D002712:Chlorides / Q000097:blood; D000242:Cyclic AMP / Q000652:urine; D006152:Cyclic GMP / Q000652:urine; D005260:Female; D005498:Follicular Phase / Q000502:physiology; D005919:Glomerular Filtration Rate; D006339:Heart Rate; D006439:Hemodynamics / Q000502:physiology*; D006801:Humans; D008183:Luteal Phase / Q000502:physiology*; D009566:Nitrates / Q000652:urine; D009573:Nitrites / Q000652:urine; D009638:Norepinephrine / Q000097:blood; D011247:Pregnancy / Q000502:physiology*; D012016:Reference Values; D012039:Regional Blood Flow; D012079:Renal Circulation / Q000502:physiology*; D012083:Renin / Q000097:blood; D012084:Renin-Angiotensin System; D012964:Sodium / Q000097:blood; D014655:Vascular Resistance; D014664:Vasodilation
chemical_list: D001639:Bicarbonates; D002712:Chlorides; D009566:Nitrates; D009573:Nitrites; D000450:Aldosterone; D009320:Atrial Natriuretic Factor; D012964:Sodium; D000242:Cyclic AMP; D012083:Renin; D006152:Cyclic GMP; D009638:Norepinephrine