Endogenous and exogenous female sex hormones and renal electrolyte handling: effects of an acute sodium load on plasma volume at rest.
This study was conducted to investigate effects of an acute sodium load on resting plasma volume (PV) and renal mechanisms across the menstrual cycle of endurance-trained women with natural (NAT) or oral contraceptive pill (OCP) controlled cycles. Twelve women were assigned to one of two groups, according to their usage status: 1) OCP [n = 6, 29 yr (SD 6), 59.4 kg (SD 3.2)], or 2) NAT [n = 6, 24 yr (SD 5), 61.3 kg (SD 3.6)]. The sodium load was administered as a concentrated sodium chloride/citrate beverage (164 mmol Na(+)/l, 253 mosmol/kgH(2)O, 10 ml/kg body mass) during the last high-hormone week of the OCP cycle (OCP(high)) or late luteal phase of the NAT cycle (NAT(high)) and during the low-hormone sugar pill week of OCP (OCP(low)) or early follicular phase of the NAT cycle (NAT(low)). The beverage ( approximately 628 ml) was ingested in seven portions across 60 min. Over the next 4 h, PV expanded more in the low-hormone phase for both groups (time-averaged change): OCP(low) 6.1% (SD 1.1) and NAT(low) 5.4% (SD 1.2) vs. OCP(high) 3.9% (SD 0.9) and NAT(high) 3.5% (SD 0.8) (P = 0.02). The arginine vasopressin increased less in the low-hormone phase [1.63 (SD 0.2) and 1.30 pg/ml (SD 0.2) vs. 1.82 (SD 0.3) and 1.57 pg/ml (SD 0.5), P = 0.0001], as did plasma aldosterone concentration ( approximately 64% lower, P = 0.0001). Thus PV increased more and renal hormone sensitivity was decreased in the low-hormone menstrual phase following sodium/fluid ingestion, irrespective of OCP usage.
Sims
Stacy T
ST
School of Physical Education, University of Otago, Dunedin, New Zealand. stsims@stanford.edu
Rehrer
Nancy J
NJ
Bell
Melanie L
ML
Cotter
James D
JD
D000328:Adult; D001127:Arginine Vasopressin / Q000378:metabolism; D001642:Bicycling / Q000502:physiology; D001834:Body Water / Q000378:metabolism; D003278:Contraceptives, Oral, Hormonal / Q000494:pharmacology; D004573:Electrolytes / Q000378:metabolism*; D004997:Ethinyl Estradiol / Q000494:pharmacology; D005260:Female; D005498:Follicular Phase / Q000502:physiology; D012739:Gonadal Steroid Hormones / Q000494:pharmacology*; D006728:Hormones / Q000502:physiology; D006801:Humans; D007668:Kidney / Q000378:metabolism*; D016912:Levonorgestrel / Q000494:pharmacology; D008183:Luteal Phase / Q000502:physiology; D015233:Models, Statistical; D009997:Osmotic Pressure; D010953:Plasma Volume / Q000187:drug effects*; D011372:Progestins / Q000494:pharmacology; D012146:Rest / Q000502:physiology*; D012964:Sodium / Q000494:pharmacology*
D003278:Contraceptives, Oral, Hormonal; D004573:Electrolytes; D012739:Gonadal Steroid Hormones; D006728:Hormones; D011372:Progestins; D001127:Arginine Vasopressin; D004997:Ethinyl Estradiol; D016912:Levonorgestrel; D012964:Sodium