Hypertension Journal

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Hypertension and Menopause
Hypertension and Menopause
1Anuj Maheshwari, 2Bharti Maheshwari
1Professor and Head, 2Professor
1Department of General Medicine, Babu Banarasi DasUniversity, Lucknow, Uttar Pradesh, India
2Department of Obstetrics and Gynecology, MuzaffarnagarMedical College, Muzaffarnagar, Uttar Pradesh, India
Correspondence Author: Anuj Maheshwari, 3/95, Vikas NagarLucknow, Uttar Pradesh, India
Phone: +919918116016
e-mail: dranujm@gmail.com
Hypertension is more common in postmenopausal femalesthan males. As they move in postmenopausal state, a normalprotection from cardiovascular (CV) disease is withdrawn andcontrol of hypertension also becomes tougher despite beingmore sincere in blood pressure (BP) monitoring and treatment.They are more affected with nondipping in night, which reflectsmore target organ damage. Renin-angiotensin system activationmay lead to postmenopausal hypertension though it is not thesole cause. Obesity is another causal factor as a component ofmetabolic syndrome, which also impacts outcome of antihypertensivetherapy in postmenopausal females. Sympathetic activationincreases BP, which is aggravated further by weight gain,increased leptin level, and age. Role of estrogen is not clear innormal protection of young females from CV risks or its low levelin postmenopausal women with hypertension. Young girls withpolycystic ovary syndrome have elevated serum androgens whichare low after menopause but increases up to premenopausal leveltill 70 years of age and correlates with body mass index only inpostmenopausal age. Increased serum testosterone correlateswith risk of type 2 diabetes mellitus in postmenopausal females.Sympathetic activation with anxiety and depression may leadto hypertension which is established with metabolic syndromealso. Angiotensin-converting-enzyme inhibitors are used for BPfor reducing anxiety and depression. Therefore, it needs differenttreatment approach for postmenopausal hypertension.
Keywords: Androgen, Anxiety, Depression, Diabetes, Estrogen,Hypertension, Menopause, Metabolic, Obesity, Renin-Angiotensinsystem.
How to cite this article: Maheshwari A, Maheshwari B.Hypertension and Menopause. Hypertens J 2017;3(1):23-26.
Source of support: Nil
Conflict of interest: None


Aging in males and females can be identified by a rise inblood pressure (BP),1-8 and the incidence of hypertensionin postmenopausal women is greater than in males,1-4with 41% of postmenopausal females being hypertensive.4Globally, 25% of adult females become hypertensive,5 and in the USA, greater than 75% of females over 60 years ofage are hypertensive.4,6,7 In trials involving the NationalHealth and Nutrition Examination Survey (NHANES)IV (1999-2004) database, the proportion of subjects withuncontrolled BP was 50.8 ± 2.1% in males and 55.9 ± 1.5%in females, in spite of the fact that more females measuredtheir BP in the last 6 months.9 Moreover, a trial thatcompared the NHANES III cohort and the NHANES IVcohort concluded that hypertension was not much controlledin females than males; however, the therapy usedto manage hypertension was same in males and females.9In addition, lesser fall of BP during night hours can becorrelated with more target organ complications in malesand females.10-14 Therefore, nondipping in females is dueto more target organ complications.10,12 Postmenopausalfemales are more affected compared with males and premenopausalfemales in nocturnal nonreduction of BP.10Therefore, however, antihypertensive medications arenot different in males and females, and females are moreprone to have their BP assessments, hypertension is likelyto be lesser managed in females. This can predict thatfemales may not be as actively managed in hypertension.


Activation of the renin-angiotensin system (RAS) canbe postulated as the process through which BP increasesin aging postmenopausal females. In postmenopausalfemales, plasma renin activity is increased,14,15 whichshows the increase in RAS activity. Moreover, in postmenopausalwomen, due to hereditary reasons, RASactivation may lead to postmenopausal hypertensionbetween the age group of 40 and 70 years; however, it isnot seen in males.16 Studies suggested that RAS activationis not the sole contributor in the postmenopausal BPincrease.16 For postmenopausal hypertension, it can bedescribed as mediator.


Obesity may be another causal factor of hypertensionin postmenopausal females.17,18 Obesity is the integralpart of the group of metabolic disorders called as themetabolic syndrome which contains insulin resistance,type 2 diabetes, dyslipidemia, and hyperleptinemia, all ofwhich are known to cause hypertension.17,18 The incidence of obesity is close to 40% in postmenopausal women.19Obesity is more prevalent and prone to increase aftersurgical menopause and in females who have been prescribedhormone replacement therapy within 12 monthsof amenorrhea.20

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Anuj Maheshwari, Bharti Maheshwari

There are also incidences where females have notgained extra weight after menopause and the body fathas been redistributed, leading to a rise in abdominalfat compared with subcutaneous fat in the hips region.21Weight that assimilates in the abdomen is responsiblefor increased prevalence of cardiovascular (CV) diseasethan weight, i.e., assimilated in the lower region of body.22Rossi et al22 concluded that decrease in endothelial dysfunctionand inflammation seen due to antihypertensivetherapy in postmenopausal females aged 47 to 60 yearswho had signs and symptoms of the metabolic disorder.Therefore, metabolic disorders may not cause only hypertensionbut may also affect the outcome of antihypertensivemedications in postmenopausal females.


Weight gain, plasma leptin levels, and increased age arethe causal factors for sympathetic activation.23-26 Moreover,studies suggested27 that the sympathetic nervoussystem has a role in increasing BP with increased weight.In addition, obesity can be correlated with increases inplasma leptin levels,23,26 and infusion of leptin rises BP inanimals.23 Inhibition of the sympathetic nervous systemmay decrease hypertensive activity,26 thereby indicatingleptin in sympathetic activation.

Leptin has been hypothesized to enhance the sympatheticnervous system via activation of melanocortin 4receptors in proopiomelanocortin neurons in the hypothalamus.24,27 Inhibition of these receptors decreases BPin obese rats.27 Such kind of studies suggested that obesityand increased leptin levels can lead to hypertension inpre- and postmenopausal females via activation of thesympathetic nervous system.


Estrogen levels are controversial in the protection againsthypertension in premenopausal females, and the effect ofdecreased estrogen levels on hypertension in postmenopausalwomen is also controversial. Olszanecka et al28evaluated ambulatory BP in normotensive and hypertensivefemales aged 40 to 60 years and concluded that thereis no difference in BP in normotensive and hypertensivesubjects irrespective of menopausal status. Coincidently,there have been no studies wherein ambulatory BP hasbeen evaluated periodically over the perimenopausal phase in order to document any BP change with menopausalphase.
It is unclear whether the estrogen levels save youngfemales from high BP or decreased estrogen levels favorendothelium-dependent, flow-mediated vasodilationhypertension in postmenopausal women. Studies concludedthat decreased estrogen level leads to endothelialdysfunction irrespective of age, and is prevalent inpopulation with high BP. Young females with polycysticovary syndrome have increased levels of plasma androgenswith normal plasma estradiol levels, which can becorrelated with elevated risk of CV disease in pre- andpostmenopausal periods.28-30 Studies have concludedthat serum androgens are low after menopause, but till70 years of age, they are gradually increased to levels foundin premenopausal women.31 The ovary in postmenopausalfemales is a main contributor of androgens;32,33however, studies concluded that nonproductive tissueslike kidney also produce androgen.34 Moreover, in postmenopausalfemales, serum androgen levels increasewith increase in body mass index (BMI); on the contrary,it has not been seen with premenopausal females.35 Inaddition, with increases in BMI and obesity, androgenlevels have also been decreased in males.36

Moreover, increased serum testosterone levels canbe correlated with increased risk of type 2 diabetes inpostmenopausal females, on the contrary, not seen inage-matched males.37


Anxiety and depression may be the risk factors forhypertension, and it has been seen that females who arehypertensive may have increased incidences of anxietyand depression. Depression and anxiety incidencesoccur at much increased rate in females than in males.38Depression and anxiety can be correlated with increasedrisk of CV disease and other metabolic disorders. Forinstance, patients with bipolar abnormalities have anadded risk of hypertension.39 Sympathetic activity canbe upregulated with anxiety and chronic mental stress,which may lead to hypertension. This correlation hasbeen established in patients with metabolic syndromeand hypertension.40 Increased BP was also seen due toenhanced levels of anxiety in a small Spanish cohort.41Moreover, angiotensin-converting-enzyme inhibitorsused for the management of hypertension have been seento decrease the incidence of depression with anxiety.42The mechanisms pertaining to the cause of chronicanxiety and depression and its correlation to hypertensionin postmenopausal females are not clear and shouldbe studied further.

Hypertension and Menopause


Hypertension in postmenopausal females has manyetiologies and risk factors. Females are much more compliantto the advice of health-care providers and stick totheir pharmacotherapy. On the contrary, hypertensionin this group is not very well-controlled compared withage-matched men, which suggests that different pathophysiologicmechanisms may be involved and differentmanagement approach is required compared with thestrategies that are successful in men, for the managementof hypertension in postmenopausal females.

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