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there is a normative inverse relationship between sodium intake (and sodium


excretion) and PRA, angiotensin II, and aldosterone levels (whether measured in


serum or urine) such that when the hormones are relatively elevated sodium and


fluid is retained by the kidney, and when they are low, there is an increase in


excretion (see Sealey and Laragh 1995 ). However, excessive sodium andfluid


retention in conjunction with increased PRA, angiotensin II, and aldosterone levels


can lead to substantially increased circulating plasmafluid volume, which will, in


turn, increase blood pressure often to the point of hypertension (Sealey and Laragh


1995 ).


Numerous studies have shown that in pre-menopausal women, PRA and


aldosterone levels are substantially elevated in the luteal phase relative to the fol-


licular phase of the menstrual cycle (e.g., James and Marion 1994 ; Chapman et al.


1997 ; Stachenfeld et al. 1999 ; Chidambaram et al. 2002 ; Pechere-Bertschi and


Burnier 2004 ), and given the normative physiological expectations noted above,


sodium andfluid should be (and apparently are) retained in the luteal phase (see


Reid and Yen 1981 ), and blood pressure should also be increased relative to the


follicular phase as a consequence. However, there are numerous studies showing


that there is little to no change in circadian blood pressure levels from the follicular


to luteal phase in pre-menopausal women (e.g., Karpanou et al. 1993 ; James and


Marion 1994 ; Williamson et al. 1996 ; Pechere-Bertschi and Burnier 2004 ;
Arifuddin et al. 2012 ), and research further indicates that the blood pressure of


pre-menopausal women is relatively insensitive to variation in dietary salt intake


regardless of when it is measured during the menstrual cycle (Pechere-Bertschi and


Burnier 2004 ). Several factors may contribute to the apparent attenuation of the


effects of the RAAS during the cycle, including potential counteractive effects of


estrogen and progesterone which promote vasodilation and aldosterone receptor


antagonism (e.g., Pechere-Bertschi and Burnier 2004 ; Arifuddin et al. 2012 ) as well


as increases in renal bloodflow, vasodilation, glomerularfiltration rate, and relative


distal nephron sodium reabsorption that are unrelated to the actions of the RAAS


(Chapman et al. 1997 ; Pechere-Bertschi et al. 2002 ). Table8.1 shows blood


pressure, PRA, and urinary aldosterone variation from the mid-follicular to


mid-luteal phase of the cycle in an ethnically diverse sample of 47 women who all


worked as secretaries and technicians at a hospital in New York City. Table8.2


shows selected characteristics of the women. Note that blood pressure similarities


between the phases occur not only on average over the whole day, but also within


each daily microenvironment—at work, at home, and during sleep. Similarly, luteal


urinary aldosterone levels are greater over the whole day as well as in each daily


microenvironment (work, home, and sleep).


The question arises as to why there is this“hidden”attenuation of the RAAS in


cycling women in terms of blood pressure regulation. The explanation may lie in


the fact that the menstrual cycle occurs for the purpose of reproduction, which


requires thatfluid volume be retained during the luteal phase to facilitate egg


implantation in the uterus (under the assumption that an egg will be fertilized and


the woman will become pregnant) (Reid and Yen 1981 ). When she does not, the


158 G.D. James

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