The effect of intrauterine devices, oral contraceptives, estrogens, and progestogens on blood pressure

Spellacy, William N.; Birk, S.A.

doi:10.1016/0002-9378(72)90811-3

Cited by 94 publications

(28 citation statements)

References 12 publications

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“…Rabbits pretreated with progesterone have been shown to have increased arterial pressures (12) and potentiated pressor responses to aldosterone (16). On the other hand, hyperten sion has been found only in women taking estrogens but not in those taking progestogens (25). Our results may indicate species differences since on weeks 10 and 19 of the second group of experiments (see table II), the Enovid-treatcd rats had significantly higher pressures than those given corn oil, mestranol, or norethynodrel.…”

Section: Discussioncontrasting

confidence: 39%

Potentiation of Hypothalamic Pressor Responses in Awake Rats Pretreated with Contraceptive Steroids

1975

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Contrasting with the hypertension resulting consistently after DOCA implantation, mature female rats given Enovid daily for 20 weeks had only slight and occasional increases in blood pressure. The pressure elevations remained infrequent and transient even when drinking water was replaced with isotonic saline solution but they became more pronounced when Enovid treatment was initiated at an earlier age. Despite the failure to cause sustained hypertension, the data indicate that Enovid affects blood pressure and that both mestranol and norethynodrel are essential for this effect. Pressor responses to norepinephrine or angiotensin were unaffected even after 20 weeks of pretreatment but those to electrical stimulation of the posterior hypothalamus were increased in rats pretreated with Enovid. Enhanced responsiveness to hypothalamic stimulation occurred only in the awake state and was not demonstrable after the central nervous system (CNS) had been depressed with urethane. These results can be explained by an increased sensitivity of hypothalamic pressor areas produced by Enovid prior to the development of hypertension and the mechanisms involved may be similar to those occurring in spontaneously-hypertensive rats. However, the possibility of hypersensitivity at other sites in the sympathetic vasomotor outflow cannot be ruled out.

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Section: Discussioncontrasting

confidence: 39%

Potentiation of Hypothalamic Pressor Responses in Awake Rats Pretreated with Contraceptive Steroids

1975

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“…31,[36][37][38] Contraceptive preparations tend to differ from 'postmenopausal replacement' regimens in that they consist of combinations of the 'potent' semisynthetic oestrogens ethinyloestradiol or mestranol, often with the relatively androgenic C19 progestogens, both administered in doses in excess of those used in HRT. 60 The relatively higher doses and potency of the preparations used in oral contraceptive formulations may therefore influence the effects on the vasculature and blood pressure.…”

Section: Discussionmentioning

confidence: 99%

“…Collectively, previous studies have variably shown no change, 1-12 a decrease 1,2,[13][14][15][16][17][18][19][20][21][22][23][24][25][26][27][28][29] or an increase 4,9,11,21,[30][31][32][33][34][35] in blood pressure with various combinations of HRT. Unfortunately, few of the previous studies have been designed to differentiate between the effects on blood pressure of the individual oestrogen ('natural', conjugated equine or semisynthetic) and progestogen (C21 or C19 derivatives administered as cyclical or continuous therapy) components of the regimen when these preparations have been administered in combination.…”

Section: Introductionmentioning

confidence: 99%

“…From these studies there is little evidence to suggest that contraceptive doses of progestogens given alone to normotensive premenopausal women are associated with a pressor effect on blood pressure. 31,[36][37][38] However, results of some studies have suggested that, while progestogen administered alone does not have a demonstrable pressor effect, when administered in combination with oestrogen in combined contraceptive formulations the progestogen may have a synergistic effect, thereby enhancing the pressor effect of the oestrogen. 37,39 From the currently available data a number of questions remain unanswered.…”

Section: Introductionmentioning

confidence: 99%

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Dose response effect of cyclical medroxyprogesterone on blood pressure in postmenopausal women

et al. 2001

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Objective: This study was designed to compare with placebo the dose-response effect of cyclical doses of the C21 progestogen, medroxyprogesterone acetate (MPA) on blood pressure (BP) when administered to normotensive postmenopausal women receiving a fixed mid-range daily dose of conjugated equine oestrogen (CEE). Materials and methods: Twenty normotensive postmenopausal women (median age 53 years) participated in the study which used a double-blind crossover design. There were four randomised treatment phases, each of 4 weeks duration. The four blinded treatments were MPA 2.5 mg, MPA 5 mg, MPA 10 mg and matching placebo, taken for the last 14 days of each 28 day treatment cycle. CEE 0.625 mg was also administered once daily as open labelled tablets to all subjects throughout the study. Clinic BP was measured weekly with the

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“…1215 The effect of oral contraceptives of varying composition on blood pressure is shown in Table 1. The study of Spellacy and Birk 16 was prospective and involved 415 normotensive women observed over a 6-to 12-month period. The development of diastolic hypertension while taking oral contraceptives was significantly higher if the women had hypertension in a pregnancy previously.…”

Section: Role Of Estrogen Versus Progestogen In Cardiovascular Complimentioning

confidence: 99%

Oral contraceptives and hypertension.

Woods

1988

Hypertension

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IT is generally accepted that use of oral contraceptives is etiologically related to a rise in blood pressure. Support for this premise has come from case reports and cross-sectional and longitudinal studies as well as from animal experiments. In this review, answers to the following questions are sought: 1) What is the incidence and severity of the hypertension? 2) Does the hypertension underlie other known complications of oral contraceptives, such as stroke and myocardial infarction? 3) Which component or components of oral contraceptives are responsible and in what dosage? 4) What is the mechanism whereby oral contraceptives elevate blood pressure? 5) Which groups of women are at particular risk? 6) Are there experimental models in which the problem can be studied? 7) What should the general prescribing policy be? IncidenceOral contraceptives became generally available in the early 1960s. During this period, their use increased rapidly, and by 1977, it was estimated that about 54 million women were using them worldwide. Since the mid 1970s, publicity regarding complications (primarily the increase in the risk of cardiovascular disease) has undoubtedly been responsible for the decline in their use in the United States. Analysis of these complications is made difficult by the large number of publications involving small numbers of subjects, the absence of suitable controls in many reports, the varying composition of preparations in past and present use, and the fact that some combinations of estrogen and progestogen act synergistically and others an- tagonistically. Consequently, differing conclusions abound in the literature on this subject. Here, an attempt will be made at a synthesis and overview of major findings and not a critique of the methodological strengths and weaknesses of the various studies cited.By 1963, case reports of thromboembolic disease in . women using oral contraceptives were numerous, and by 1967, the first reports 12 suggesting an association between oral contraceptives and hypertension appeared. The incidence in early studies varied widely. For example, Tyson 3 found that 15.5% of 45 women taking oral contraceptives developed an elevated blood pressure and Saruta and colleagues 4 found elevated pressure in 18% of 56 women. In the prospective study of Weir and co-workers, 5 83 users of oral contraceptives were observed and compared with a control group that used mechanical methods of birth control over a 3-year period. Increases were found in mean systolic and diastolic blood pressures of 9.2 and 5.0 mm Hg, respectively. After an additional year, in a smaller group, the mean rise in systolic pressure was 14.2 mm Hg and in diastolic pressure, 8.5 mm Hg. Blood pressure returned to pretreatment levels within 3 months after hormonal therapy was stopped. Clezy and coworkers 6 in Australia, using a blood pressure of greater than 150/90 mm Hg as the definition of hypertension, observed that 4% of 74 women developed hypertension.

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The effect of intrauterine devices, oral contraceptives, estrogens, and progestogens on blood pressure

Cited by 94 publications

References 12 publications

Potentiation of Hypothalamic Pressor Responses in Awake Rats Pretreated with Contraceptive Steroids

Potentiation of Hypothalamic Pressor Responses in Awake Rats Pretreated with Contraceptive Steroids

Dose response effect of cyclical medroxyprogesterone on blood pressure in postmenopausal women

Oral contraceptives and hypertension.

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