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