Effects of estrogen replacement therapy on natriuretic peptides and blood pressure

Karjalainen, Anna; Ruskoaho, Heikki; Vuolteenaho, Olli; Heikkinen, Jorma; Bäckström, A C; Savolainen, Markku J.; Kesäniemi, Y. A.

doi:10.1016/s0378-5122(03)00279-2

Cited by 36 publications

(20 citation statements)

References 31 publications

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“…In the present study, the systolic blood pressure in the OVX rats was within normal limits, though it was significantly higher than in sham rats; the increase in SBP could be reversed by estrogen treatment. This is consistent with previous reports that transdermal estrogen can lower blood pressure, while the effects of oral estrogens tend to be neutral [17,18].…”

Section: Discussionsupporting

confidence: 93%

Effects of ovariectomy and 17β-estradiol treatment on the renin–angiotensin system, blood pressure, and endothelial ultrastructure

Xiao

Luo

et al. 2008

International Journal of Cardiology

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Section: Discussionsupporting

confidence: 93%

Effects of ovariectomy and 17β-estradiol treatment on the renin–angiotensin system, blood pressure, and endothelial ultrastructure

Xiao

Luo

et al. 2008

International Journal of Cardiology

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“…This preparation was selected for the study as it is the most common dose and preparation of endogenous human estrogen prescribed as an oral preparation and one that has been documented to consistently lower BP in healthy normotensive postmenopausal women. 6,7,[15][16][17][18] After the second study day, women with a uterus in situ were prescribed medroxyprogesterone acetate 10-mg tablets once daily for 12 days to convert the endometrium from the follicular to the secretory state.…”

Section: Protocolmentioning

confidence: 99%

“…11 This hypothesis would explain the very modest blood pressure (BP) elevation noted with premenopausal contraceptive estrogen administration 2 and its absence and even BP reduction noted in some postmenopausal women receiving ERT. 3,7,12,13 However, a recent study by Chidambaram et al, which examined the RAS at different phases of the menstrual cycle, showed increased renin, plasma renin activity, and aldosterone during the high estrogen-progestin luteal phase (days 15 to 24) when compared with the low estrogen-progestin early follicular phase (days 3 to 6) of the menstrual cycle. 14 Furthermore, the luteal phase was associated with an augmented renin, angiotensin II, and aldosterone response to simulated orthostatic stress.…”

mentioning

confidence: 99%

“…1 Administration of exogenous estrogen to premenopausal women in contraceptive formulations 2 and to postmenopausal women as estrogen replacement therapy (ERT) 3 increases plasma concentrations of this renin substrate. Furthermore, estrogen administration for these purposes has been shown to increase plasma angiotensin II, 2,4,5 with either no change 3,6,7 or a decrease in plasma renin 3,7 and a concurrent decrease in angiotensin-converting enzyme (ACE) activity. 5,8 Conversely, estrogen deficiency has been associated with augmentation of ACE synthesis and activity 9 and upregulation of the angiotensin II type 1 (AT 1 ) receptor, 10 the primary mediator of the hemodynamic, endocrine, and mitogenic actions of angiotensin II.…”

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confidence: 99%

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Estradiol Induces Discordant Angiotensin and Blood Pressure Responses to Orthostasis in Healthy Postmenopausal Women

et al. 2005

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Postmenopausal estrogen replacement therapy (ERT) is reported to increase angiotensin II under resting conditions. To determine the implications of this increase for cardiovascular regulation during simulated orthostasis, blood pressure (BP), heart rate (HR), renin, angiotensinogen, angiotensin II, and aldosterone were measured at rest and during lower body negative pressure (LBNP; -10, -20, and -40 mm Hg). We studied 13 normotensive postmenopausal women (54+/-2 [mean+/-SE] years) before and after 1 month of oral estradiol 2 mg daily, and 14 premenopausal women. LBNP activated the renin-angiotensin system acutely in premenopausal but not postmenopausal women. Resting renin and aldosterone were unaffected by estradiol, whereas angiotensinogen (P<0.001) and angiotensin II (P<0.01) increased. Renin, aldosterone, and HR responses to LBNP (which tended to be less in postmenopausal women [P=0.06]) were not affected by estradiol. Importantly, angiotensin II was higher on estradiol during all stages of LBNP, and increased 70% above resting values at the end of this stimulus (P<0.05), yet BP was significantly lower, both at rest (P<0.05) and during LBNP (P<0.01). In summary, in normotensive postmenopausal women, estradiol increases angiotensin II, but not aldosterone, at rest and during orthostatic stress, yet lowers, rather than raises, BP under both conditions. Downregulation of vascular and adrenal responsiveness to angiotensin II may protect healthy women against this activation. Loss of such protection may elevate BP and have adverse implications for women with conditions that impair their capacity to counteract the pathological actions of angiotensin II. This may contribute to higher cardiovascular event rates reported in recent ERT trials.

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“…Some clinical studies have demonstrated that estrogens, administered for contraception in pre-menopausal women (5) or as hormone replacement therapy in post-menopausal women (17,18), increase the circulating levels of BNP and NT-proBNP. Moreover, androgen receptor blockade, and to a lesser extent, androgen suppression cause an increase in NT-proBNP levels in men with prostate cancer (19).…”

Section: See Page 618mentioning

confidence: 99%

When Gonads Talk to the Heart

Clerico¹,

Passino²,

Emdin³

2011

Journal of the American College of Cardiology

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Pisa, ItalyCardiovascular risk is significantly lower in normally cycling women compared with men. This difference is abolished after menopause, suggesting a link with sex steroid hormones. Early studies on cardiac endocrine function disclosed higher natriuretic peptide concentrations in women than in men, suggesting the hypothesis that female sex steroid hormones could directly stimulate cardiomyocyte hormone production and secretion (1). Kuroski de Bold (2) hypothesized that an improved cardiovascular risk profile in cycling women could be associated with some estrogen stimulatory effect on cardiac endocrine function. Indeed, cardiac natriuretic peptides exert several protective actions on the heart and vessels, including: 1) vasodilatation; 2) promotion of diuresis/natriuresis; and 3) inhibition of hypertrophy, fibrosis, and apoptosis either directly or via inhibition of the sympathetic and renin-angiotensin-aldosterone systems, as well as the release or action of endothelin and vasopressin (1). See page 618More recently, 3 large population-based studies have indicated that male sex steroid hormones might modulate cardiac endocrine function too (3)(4)(5). These studies demonstrated a significant inverse association between the circulating levels of B-type natriuretic peptide (BNP) or N-terminal fragment of pro-B-type natriuretic peptide (NT-proBNP) and male sex steroid hormones (i.e., total and free testosterone) in both sexes (3-5), whereas the association with estradiol was found to be weak or not significant at all (3,4). Furthermore, these studies reported that levels of sex hormone-binding globulin (SHBG) are positively associated with NT-proBNP levels in both male and female adolescents (4), as well as in adult women (3,5) and men (5). Testosterone and estradiol circulate in the bloodstream mostly bound to SHBG, with levels that directly influence bioavailability of sex hormones; only a small fraction of total steroid concentration is unbound or "free" (1% to 5%) and biologically active (i.e., able to enter a cell and activate its receptors).Lam et al. (5), in this issue of the Journal, evaluate plasma NT-proBNP, total testosterone, and SHBG concentrations in 4,056 adult men and women from the Framingham Heart Study Third-Generation Cohort; estradiol was not measured. They found lower NT-proBNP plasma levels in men than in age-matched women and higher NT-proBNP levels in women receiving hormonal contraceptives than in women who were not (5). Moreover, serum free (non-protein-bound) testosterone was positively and serum SHBG was negatively related to circulating NT-proBNP levels (5). The investigators suggested the hypothesis that androgens suppress NT-proBNP and that differences in free testosterone levels may largely explain the sex-and hormone-related differences in circulating levels of natriuretic peptides. They concluded that lower levels of circulating androgens and the potentiating effect of exogenous female hormone therapy contribute to the higher circulating NT-proBNP levels in women.These findi...

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Effects of estrogen replacement therapy on natriuretic peptides and blood pressure

Cited by 36 publications

References 31 publications

Effects of ovariectomy and 17β-estradiol treatment on the renin–angiotensin system, blood pressure, and endothelial ultrastructure

Effects of ovariectomy and 17β-estradiol treatment on the renin–angiotensin system, blood pressure, and endothelial ultrastructure

Estradiol Induces Discordant Angiotensin and Blood Pressure Responses to Orthostasis in Healthy Postmenopausal Women

When Gonads Talk to the Heart

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