Hypertensive Postmenopausal Women Research Articles

Ghrelin and Bone Mass in Postmenopausal Hypertensive Women

Background: Ghrelin, a recently discovered peptide mainly secreted by the stomach, has an orexigenic effect which stimulates secretion of the growth hormone. It also has vasodilator effects which reduce blood pressure and stimulate in vitro, bone formation. Objectives: To evaluate the effect of ghrelin on bone mass and bone remodeling markers in postmenopausal hypertensive women. Material and Methods: 25 postmenopausal hypertensive women, light to moderate based on the JNC-VII criteria, were studied. They had a mean age of 58 ± 8 years, a body mass index of 28 ± 6 and a hypertension development time of 65 ± 84 months. Osteocalcin, PTHi, 25-vitamin D, ghrelin in serum and deoxypiridinoline in urine were determined in all patients. A lumbar spine densitometer was made (DXP Lunar, Madison, Wisc., USA). Results: Diminished levels of ghrelin were observed in the osteoporotic group (40 ± 19 vs. 78 ± 40, p = 0.027). When the patients were separated according to ghrelin tertiles, a greater bone mass was observed in the upper tertiles, which was associated with a decrease in the urinary deoxypiridinoline. When the total population was analyzed, no relation between the ghrelin and bone mass was found, nor with any of the parameters of calcium metabolism. Only a statistically significant relation between ghrelin and deoxypiridinoline was observed (r = –0.428, p = 0.026). Conclusions: In postmenopausal hypertensive women, ghrelin may produce a protecting effect over bone mass through an anticatabolic mechanism manifested by a decrease of bone resorption.

Antihypertensive ffects of drospirenone and 17α-estradiol in hypertensive postmenopausal women

Antihypertensive ffects of drospirenone and 17α-estradiol in hypertensive postmenopausal women

Randomized, placebo-controlled trial of the effects of drospirenone-estradiol on blood pressure and potassium balance in hypertensive postmenopausal women receiving hydrochlorothiazide

Drospirenone (DRSP), a spironolactone analog with aldosterone antagonist activity, is a novel progestogen developed for use as hormone therapy in postmenopausal women in combination with 17beta-estradiol (E2). DRSP/E2 lowers blood pressure when used alone in hypertensive postmenopausal women or when administered concomitantly with angiotensin-converting enzyme inhibitors or angiotensin receptor blockers. DRSP/E2 has not been studied in combination with the widely prescribed hydrochlorothiazide (HCTZ). We investigated the effects of 3 mg DRSP/1 mg E2 versus placebo on blood pressure and potassium balance when added to existing therapy with 25 mg HCTZ in postmenopausal women with established stage I hypertension. This was a single-center, double-blind, randomized, placebo-controlled, two-treatment, two 4-week treatment period crossover study in 36 postmenopausal women with stage I hypertension maintained on 25 mg HCTZ. The endpoint was a change from baseline in systolic and diastolic blood pressures by 24-hour ambulatory blood pressure monitoring. Safety monitoring included serum potassium (mEq/L) and adverse events. Mean systolic and diastolic blood pressures by 24-hour ambulatory blood pressure monitoring were reduced significantly, by -7.2 and -4.5 mm Hg, respectively, with DRSP/E2 as compared with placebo. The decrease in potassium with HCTZ was 0.2 mEq/L less with DRSP/E2 than placebo, suggesting a potassium-sparing effect. The most frequently observed adverse events with DRSP/E2 were vaginal bleeding and breast tenderness, which were attributable to the hormone therapy. DRSP/E2 substantially lowers systolic and diastolic blood pressure when added to existing antihypertensive therapy with HCTZ in hypertensive postmenopausal women. In addition, DRSP/E2 has a potassium-sparing effect that counteracts HCTZ-induced potassium loss.

Drospirenone, a progestin with added value for hypertensive postmenopausal women

Drospirenone, a progestin with added value for hypertensive postmenopausal women

Effects of blood pressure reduction on cardiovascular risk estimates in hypertensive postmenopausal women

Menopause is accompanied by an increased prevalence of hypertension, which may partially explain the corresponding cardiovascular risk observed in postmenopausal women. The relationship between blood pressure and cardiovascular risk is continuous, consistent and independent of other risk factors. There are profound benefits of treating hypertension: antihypertensive therapy has been associated with large reductions in stroke, myocardial infarction and heart failure. Despite these proven benefits, hypertension is inadequately treated, or not treated at all, in the majority of patients. There has been concern regarding the use of hormone therapy in hypertensive postmenopausal women. Drospirenone/17β-estradiol, a hormone therapy, has been demonstrated to lower blood pressure in hypertensive postmenopausal women either alone or when administered simultaneously with antihypertensive drugs. This might offer a potential advantage in patients with elevated blood pressure. It is also known that the risk for target organ events extends to levels well below the established definition of 140/90 mmHg. High-normal blood pressure carries an increased cardiovascular risk when compared to lower levels of blood pressure. Identification and management of elevated blood pressure are an important component of the successful management of the postmenopausal woman and can help prevent the untoward consequences of elevated blood pressure.

Type 2 diabetes mellitus is a risk factor for the development of hypertension in postmenopausal women

Hypertension and type 2 diabetes mellitus are common diseases that are frequently found concomitantly in postmenopausal women. These findings suggest a close and/or synergistic nature in the relationship between the two disease processes; however, no prospective data exist on the incidence rate of hypertension in postmenopausal women with type 2 diabetes mellitus. The present study assessed the risk of developing hypertension in 840 postmenopausal women: 102 women (12.1% of the cohort) with type 2 diabetes mellitus and 738 (87.9%) free of diabetes. The mean +/- SD follow-up was 3.2 +/- 0.9 years (range 0.5-6.0 years). The incidence rate (cases of hypertension per 100 person-years) was 1.1 for the group of women without diabetes versus 5.6 in women with diabetes (P < 0.0001). Compared with the non-diabetic group, women with type 2 diabetes mellitus had a statistically significant higher risk of developing hypertension. The relative risks for women with diabetes was 5.09 [crude: 95% confidence interval (CI) = 3.52-7.36; P < 0.0001]; 3.43 (adjusted for body mass index and waist circumference: 95% CI = 2.25-5.14; P < 0.001); and 2.95 (adjusted for all potential confounders: 95% CI = 1.86-4.32; P < 0.01). In our prospective study, on the incidence of hypertension, the presence of type 2 diabetes was found to be a potent independent risk determinant. This suggests that postmenopausal women affected by type 2 diabetes mellitus comprise a population at high risk for the subsequent development of hypertension.

Surgical Menopause, Salt Sensitivity, and NO Bioavailability in Women

HomeHypertensionVol. 48, No. 3Surgical Menopause, Salt Sensitivity, and NO Bioavailability in Women Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessLetterPDF/EPUBSurgical Menopause, Salt Sensitivity, and NO Bioavailability in Women Kazushi Tsuda Kazushi TsudaKazushi Tsuda Division of Cardiology, Department of Medicine, Wakayama Medical University, Wakayama, Japan Search for more papers by this author Originally published7 Aug 2006https://doi.org/10.1161/01.HYP.0000237570.97050.57Hypertension. 2006;48:E12Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: August 7, 2006: Previous Version 1 To the Editor:We read with great interest the article by Schulman et al1 dealing with the association between the loss of ovarian hormones and the occurrence of salt sensitivity in healthy premenopausal women. The results of their study demonstrated that 38.7% of salt-resistant women developed salt sensitivity after surgical menopause. The authors indicated that the prevalence of salt sensitivity doubled as early as 4 months after surgical menopause. The authors proposed that the loss of ovarian function may unmask a population of women prone to salt sensitivity who would be at higher risk for the subsequent development of hypertension and cardiovascular disease.Numerous studies have shown that one of the mechanisms underlying the cardiovascular protective effect of estrogen may be the enhancement of NO production. There is evidence demonstrating that vascular endothelial function is markedly influenced by estrogen and is improved by hormone replacement therapy in postmenopausal women.2 Recently, Scuteri et al3 showed that inhibition of NO bioavailability by asymmetrical dimethylarginine ([ADMA] an endogenous NO synthase inhibitor) and a subsequent reduction in endothelial dysfunction might contribute to the increase in blood pressure during salt intake in normotensive postmenopausal women not receiving estrogen. It was also demonstrated that estrogen replacement therapy significantly reduced plasma concentration of ADMA in postmenopausal women.4 In a study that we presented earlier, it was shown that estrogen-induced improvement of membrane fluidity (the reciprocal value of microviscosity) of erythrocytes was counteracted by ADMA in postmenopausal women.5 In addition, we showed that amelioration in membrane fluidity of erythrocytes was associated with higher NO metabolite and lower ADMA levels in plasma.6 The findings might suggest that NO and ADMA might actively participate in the regulation of rheological behavior of cell membranes and microcirculation. In this context, it can be speculated that, in women with higher ADMA levels, the circulatory disorders are more pronounced. The precise role of ADMA in the development of hypertension and cardiovascular disease in women is still unclear. It is possible that estrogen deficiency after menopause might accelerate abnormalities in endothelial function by increasing ADMA levels. Therefore, we would like to know whether the plasma NO metabolite and ADMA concentrations might be associated with the changes in salt sensitivity after surgical menopause in the study by Schulman et al.1 It would be important to assess more precisely the relationship among estrogen status, salt sensitivity, and NO bioavailability in women after menopause.DisclosuresNone.1 Schulman IH, Aranda P, Raij L, Veronesi M, Aranda FJ, Martin R. Surgical menopause increases salt sensitivity of blood pressure. Hypertension. 2006; 47: 1168–1174.LinkGoogle Scholar2 Higashi Y, Sanada M, Sasaki S, Nakagawa K, Goto C, Matsuura H, Ohama K, Chyayama K, Oshima T. Effect of estrogen replacement therapy on endothelial function in peripheral resistance arteries in normotensive and hypertensive postmenopausal women. Hypertension. 2001; 37: 651–657.CrossrefMedlineGoogle Scholar3 Scuteri A, Stühlinger MC, Cooke JP, Wright JG, Lakatta EG, Anderson DE, Fleg JL. Nitric oxide inhibition as a mechanism for blood pressure increase during salt loading in normotensive postmenopausal women. J Hypertens. 2003; 21: 1339–1346.CrossrefMedlineGoogle Scholar4 Teerlink T, Neele SJ, de Jong S, Netelenbos JC, Stehouwer CD. Oestrogen replacement therapy lowers plasma levels of asymmetrical dimethylarginine in healthy postmenopausal women. Clin Sci(Lond). 2003; 105: 67–71.CrossrefGoogle Scholar5 Tsuda K, Kinoshita Y, Kimura K, Nishio I, Masuyama Y. Electron paramagnetic resonance investigation on modulatory effect of 17beta-estradiol on membrane fluidity of erythrocytes in postmenopausal women. Arterioscler Thromb Vasc Biol. 2001; 21: 1306–1312.CrossrefMedlineGoogle Scholar6 Tsuda K, Nishio I. An association between plasma asymmetric dimethylarginine and membrane fluidity of erythrocytes in hypertensive and normotensive men: an electron paramagnetic resonance investigation. Am J Hypertens. 2005; 18: 1243–1248.CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Gohar E, Kasztan M, Becker B, Speed J and Pollock D (2017) Ovariectomy uncovers purinergic receptor activation of endothelin-dependent natriuresis, American Journal of Physiology-Renal Physiology, 10.1152/ajprenal.00098.2017, 313:2, (F361-F369), Online publication date: 1-Aug-2017. Schulman I, Aranda P, Raij L, Veronesi M, Aranda F and Martin R (2006) Response to Surgical Menopause, Salt Sensitivity, and NO Bioavailability in Women, Hypertension, 48:3, (E13-E13), Online publication date: 1-Sep-2006. September 2006Vol 48, Issue 3 Advertisement Article InformationMetrics https://doi.org/10.1161/01.HYP.0000237570.97050.57PMID: 16894052 Originally publishedAugust 7, 2006 PDF download Advertisement SubjectsEtiology

Centrally acting antihypertensive drugs

The article deals with the overview of different classes of antihypertensive centrally acting drugs. Author’s own experience concerning the use of moxonidine in postmenopausal hypertensive obese women is also provided.

Rhinitis and snoring as risk factors for hypertension in post-menopausal women

Several studies have suggested an association between snoring and hypertension. An association between rhinitis and hypertension has been recently indicated in men but not in women. Since menopausal status is an important determinant of blood pressure, we evaluated the relationship between rhinitis, snoring and blood pressure taking into account the modifying effect of menopausal status. Cross-sectional survey. Four areas of Italy: the Po river Delta, Pisa (Tuscany), Viterbo (Lazio) and Rome. Data were collected by a questionnaire and a medical visit. One thousand five hundred and fifty-four female non-smokers. Systolic blood pressure (SBP) was significantly related to both occasional and habitual snoring in the overall sample. No associations were found between SBP, snoring, and rhinitis in pre-menopausal women. Both occasional and habitual snoring, but not rhinitis, were significant risk factors for increased SBP in women who stopped menstruating fewer than 11 years previously (beta=10.27 mmHg, 95% confidence interval (CI)=3.5, 17.01 and beta=9.91 mmHg, 95% CI=2.3, 17.5, respectively). However, women who had been menopausal for more than 11 years were found to have an increased SBP if they were occasional snorers (beta=8.94 mmHg 95% CI=1.2, 16.6) or habitual snorers (beta=8.01 mmHg, 95% CI=0.10, 15.9). The increase in SBP was even greater in these women when habitual snoring was associated with rhinitis (beta=11.96 mmHg, 95% CI=1.01, 22.9). We suggest that the association of snoring with rhinitis may facilitate the development of apnea during sleep, which in post-menopausal women may increase the risk of developing hypertension.

Endometrial thickness in asymptomatic postmenopausal Nigerian women with and without hypertension

Hypertension has been identified as a risk factor for the development of endometrial carcinoma. Assessment of endometrial thickness using endovaginal ultrasonography has proved useful in the diagnosis of pathologic endometrial changes in postmenopausal women. Granberg et al. documented that if the cut-off limit for an abnormally thick endometrium was set at 5 mm the positive predictive value for identifying pathologic changes was 87.3%. Studies performed outside Nigeria have shown that compared with normotensive postmenopausal women hypertensive postmenopausal women had increased asymptomatic endometrial thickness. (excerpt)

Effects of estradiol alone and combined with norethisterone acetate on pulse-wave velocity in hypertensive postmenopausal women

Background. Arterial hypertension and postmenopausal reduction of estrogen levels may be involved in modifications of the stiffness of large arteries.Objectives. To evaluate the pulse-wave velocity (PWV) and indirectly the arterial stiffness in hypertensive postmenopausal women submitted to hormone therapy with estradiol alone or combined with norethisterone acetate.Subjects. Forty-five hypertensive postmenopausal women were double-blindly, randomly assigned to three arms of treatment: placebo (group I); estradiol 2 mg/day (group II); or estradiol 2 mg/day and norethisterone acetate 1 mg/day (group III).Methods. Arterial stiffness was assessed from PWV measurements of the common carotid and femoral arteries (CF-PWV) and the common carotid and radial arteries (CR-PWV) obtained using the automatic Complior® device, taken at baseline and after 12 weeks of treatment.Results. After the 12-week treatment, values of CF-PWV and CR-PWV were not significantly different (p = 0.910 and p = 0.736, respectively) among the groups. Systolic blood pressure showed a positive correlation with CF-PWV in groups II and III (p = 0.02 and p < 0.001, respectively).Conclusions. PWV and arterial stiffness in postmenopausal hypertensive women did not reduce over a 12-week treatment with estradiol alone compared with the same period of treatment with estradiol combined with norethisterone acetate.

Hypertension in Postmenopausal Women

Hypertension in Postmenopausal Women

Hypertension in Postmenopausal Women

Hypertension in Postmenopausal Women

The long-term effects of low-dose 17β-estradiol and dydrogesterone hormone replacement therapy on 24-h ambulatory blood pressure in hypertensive postmenopausal women: a 1-year randomized, prospective study

Objective The aim of this study was to assess the long-term effects of low-dose oral hormone replacement therapy (HRT) on 24-h blood pressure in hypertensive postmenopausal women.Study design In this 12-month, prospective study, 66 postmenopausal women with mild or moderate hypertension were randomly assigned to receive either HRT with 1 mg/day micronized 17β-estradiol sequentially combined with 10 mg/day dydrogesterone for 14 days of each 28-day cycle, or no therapy. Ambulatory blood pressure measurements were recorded for a 24-h period at baseline and after 12 months of treatment or follow-up.Results Blood pressure did not differ significantly between the groups at baseline. After 12 months, there were falls in 24-h systolic, diastolic and mean arterial blood pressure in both the HRT and control groups; only the fall in mean arterial blood pressure in the HRT group achieved statistical significance (−2.0 ± 0.8 mmHg, p < 0.01). While there was no significant decrease in daytime systolic or mean arterial blood pressure in either group, a significant decrease in diastolic blood pressure (−1.8 ± 10 mmHg, p < 0.001) was observed in the HRT group. Night-time systolic and mean arterial blood pressure also decreased significantly (p < 0.001) in the HRT group (−3.0 ± 1.5 mmHg and −2.2 ± 0.6 mmHg, respectively), but no significant change was observed in the control group.Conclusion Low-dose oral HRT caused significant falls in both daytime and night-time ambulatory blood pressure in postmenopausal women with mild or moderate hypertension.

Can drospirenone with 17-β estradiol safely reduce blood pressure in hypertensive postmenopausal women?

Can drospirenone with 17-β estradiol safely reduce blood pressure in hypertensive postmenopausal women?

A Selective Estrogen Receptor Modulator, Tamoxifen, and Membrane Fluidity of Erythrocytes in Normotensive and Hypertensive Postmenopausal Women: An Electron Paramagnetic Resonance Investigation

Recent studies have shown that tamoxifen, which belongs to a group called selective estrogen receptor modulators (SERM), may exert protective effects against cardiovascular diseases and stroke in postmenopausal women. On the other hand, abnormalities in physical properties of the cell membranes may underlie the defects that are strongly linked to hypertension, stroke, and other cardiovascular diseases. The present study was performed to investigate the effects of tamoxifen on cell membrane fluidity (a reciprocal value of membrane microviscosity) in normotensive and hypertensive postmenopausal women. We used an electron paramagnetic resonance (EPR) and spin-labeling method. Tamoxifen significantly decreased the order parameter (S) for 5-nitroxide stearate (5-NS) and the peak height ratio (h(o)/h(-1)) for 16-NS obtained from EPR spectra of erythrocyte membranes in normotensive postmenopausal women (mean +/- SEM, order parameter value; control 0.719 +/- 0.002, n = 41; tamoxifen 1 x 10(-7) mol/L 0.704 +/- 0.002, n = 41, P < .0001; tamoxifen 1 x 10(-6) mol/L 0.696 +/- 0.002, n = 41, P < .0001; tamoxifen 1 x 10(-5) mol/L 0.692 +/- 0.002, n = 41, P < .0001). The finding indicated that tamoxifen increased the membrane fluidity and improved the membrane microviscosity of erythrocytes. The membrane action of tamoxifen was antagonized by the estrogen receptor antagonist ICI 182,780. The effect of tamoxifen was significantly potentiated by the nitric oxide (NO) donors, l-arginine and S-nitroso-N-acetylpenicillamine, and a cGMP analog 8-bromo-cGMP. In contrast, the change evoked by tamoxifen was counteracted by the NO synthase inhibitors N(G)-nitro-l-arginine-methyl-ester and asymmetric dimethyl-l-arginine. In hypertensive postmenopausal women, the membrane fluidity of erythrocytes was significantly lower than in normotensive postmenopausal women. The effect of tamoxifen on the membrane fluidity was more pronounced in hypertensive postmenopausal women than in normotensive postmenopausal women. These results showed that tamoxifen increased the membrane fluidity of erythrocytes and improved the rigidity of cell membranes in postmenopausal women, to some extent, through the NO- and cGMP-dependent mechanisms. Furthermore, the greater effect of tamoxifen in hypertensive postmenopausal women suggests that tamoxifen could have a beneficial effect in regulating the blood rheologic behavior and in the improvement of the microcirculation in hypertension.

Conjugated estrogen plus medroxyprogesterone does not impair blood rheological properties in hypertensive postmenopausal women

Objectives Hypertension and estrogens are both prothrombotic. We used the microchannel method to investigate whether hormone replacement therapy (HRT) with conjugated equine estrogen (CEE) plus medroxyprogesterone acetate (MPA) affects blood flow through the microchannels in hypertensive postmenopausal women being treated with antihypertensive drugs and in normotensive postmenopausal women. Methods Sixty-two consecutive postmenopausal women were randomly assigned to a hypertensive HRT group ( n = 16), hypertensive control group ( n = 15), normotensive HRT group ( n = 16) and normotensive control group ( n = 15). Each HRT group received CEE 0.625 mg plus MPA 2.5 mg daily orally for 12 months. Both hypertensive groups were being treated with antihypertensive drugs before the study. Microvascular blood flow was assessed on the basis of blood passage time, the time required for 100 μl of whole blood to pass through a cylinder, was determined before and 12 months after the start of HRT by the microchannel method (micro channel array flow analyzer). Results CEE plus MPA therapy did not change blood passage time in any of the groups. Microscopic observation showed that the whole blood passed smoothly through the microchannels in every group. Conclusions CEE plus MPA therapy may not impair blood flow through the microchannels in hypertensive postmenopausal women receiving antihypertensive drugs or in normotensive postmenopausal women. However, administration of CEE plus MPA to postmenopausal women with hypertension warrants caution against the occurrence of thromboembolic events.

Endothelial dysfunction: its role in hypertensive coronary disease

Coronary artery disease is the major cause of death worldwide. Hypertension is a major risk factor for developing coronary disease. It is now recognized that endothelial dysfunction is an early marker of coronary artery disease before structural changes to the vessel wall are apparent on angiography or intravascular ultrasound and that it has a prognostic value in predicting cardiovascular events in hypertensive patients. This review addresses recent developments in hypertension-induced endothelial dysfunction. Hyperaldosteronism causes endothelial dysfunction independent of high blood pressure. Exaggerated exercise blood pressure response has been related to endothelial dysfunction. Cyclosporin-A-induced endothelial dysfunction is related to reduced cholesterol content in caveolae. Chronic kidney disease induces changes in caveoli-1 and thus contributes to the reduced nitric oxide bioavailability, and causes oxidative stress independent of the high blood pressure. Asymmetric dimethylarginine plays a role in endothelial dysfunction in hypertensive patients independent of insulin resistance. 20-Hydroxyeicosatetraenoic acid is an independent predictor of hypertension in postmenopausal women. Endothelial dysfunction precedes and predicts the development of hypertension in postmenopausal women. Oral treatment with L-arginine improves endothelial dysfunction in hypertensives and lowers the blood pressure. The pathophysiology of endothelial dysfunction in hypertension is multifactorial. Recent findings have contributed to our understanding of mechanisms of endothelial dysfunction and support a role for early intervention to prevent irreversible vascular and organ damage.

Effects of Drospirenone/17-β Estradiol on Blood Pressure and Potassium Balance in Hypertensive Postmenopausal Women

Drospirenone (DRSP) is a novel progestin with aldosterone receptor antagonist activity developed for hormone therapy as DRSP /17-beta estradiol (DRSP/E2). Because of a significant aldosterone antagonist activity, we studied the effects of DRSP/E2 on serum potassium (K) and blood pressure (BP) in hypertensive postmenopausal women with and without diabetes mellitus. This was a multicenter trial in postmenopausal women 44 to 70 years of age, either with type 2 diabetes mellitus (n = 82) or without type 2 diabetes mellitus (n = 148) and using an angiotensin-converting enzyme (ACE) inhibitor or angiotensin II receptor antagonist. Patients were randomized to 28 days of DRSP/E2 or placebo. Study endpoints were the number and percentage subjects who developed hyperkalemia (K >or= 5.5 mEq/L) and changes from baseline in clinic systolic and diastolic BP. To increase the likelihood of unmasking hyperkalemia, the nondiabetic group was also administered ibuprofen for 5 days. There were no statistical differences in the overall number and percentage of subjects with hyperkalemia for DRSP/E2 versus placebo. No subject had symptoms or electrocardiographic changes related to hyperkalemia. Blood pressure was reduced by -8.6/-5.8 mm Hg in patients receiving DRSP/E2 versus -3.7/-2.9 mm Hg in those receiving placebo (P < .01 for both SBP and DBP). In hypertensive postmenopausal women, treatment with DRSP/E2 was not associated with a greater incidence of hyperkalemia than with placebo in patients with and without type 2 diabetes mellitus and concomitant use of ACE inhibitors, angiotensin receptor antagonists, or ibuprofen. Furthermore, DRSP/E2 was found to have a significant antihypertensive effect in this high-risk population.

Nondipping Status Does Not Attenuate the Conjugated Estrogen-Induced Improvement in Aortic Stiffness in Postmenopausal Women with Untreated Hypertension

Whether the blunted nocturnal blood pressure (BP) fall alters the potential beneficial effects of estrogen replacement therapy (ERT) on arterial elastic properties in hypertensive postmenopausal women has not been clarified. The aim of this study was to determine the potential beneficial effects of ERT on arterial elastic properties and to investigate whether a blunted nocturnal BP fall could unfavorably modify the estrogen-induced alterations of large-artery stiffness in postmenopausal women with untreated essential hypertension. A total of 66 postmenopausal women with untreated essential hypertension underwent carotid-femoral pulse wave velocity (PWV) measurements at baseline and after 12 weeks of ERT with 0.625 mg conjugated estrogen. By 24-h ambulatory BP monitoring, women were classified according to dipping status (nondippers, n = 21; dippers, n = 45). The two groups were similar regarding age, body mass index, time since menopause, and lipidemic profile. Initially, nondippers compared to dippers, although they had significantly greater office systolic BP (SBP), 24-h SBP, daytime SBP and night-time SBP (by 5, 2, 3, and 19 mm Hg, respectively, P < .05 for all cases), did not differ regarding left ventricular (LV) mass index and aortic PWV (116 v 114 g/m2 and 8.40 v 7.95 cm/sec, respectively, P = NS for both cases). Use of ERT, without affecting the office SBP and DBP, reduced significantly the aortic PWV in both nondippers and dippers (by 1.28 and 1.50 cm/sec, respectively, P < .05 for both cases). However, these PWV reductions were not different between the two groups (P = NS). A multivariate analysis identified patient age and 24-h SBP as significant determinants of estrogen-induced aortic PWV reduction (P < .05). A blunted nocturnal BP fall does not attenuate the estrogen-induced favorable modifications of large artery elastic properties in hypertensive postmenopausal women. Whether these findings suggest that hypertensive women with ERT-induced attenuation of PWV represent a specific clinical subgroup of patients with possible ERT-associated cardiovascular benefit remains to be determined by properly randomized trials.