Blood pressure in women taking oral contraceptives

Weir, R. J.

doi:10.1016/s0002-8703(76)80411-5

Cited by 26 publications

(13 citation statements)

References 11 publications

(1 reference statement)

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“…Orally administered oestrogens, in particular conjugated equine oestrogens, increase plasma levels of renin substrate (angiotensinogen), plasma renin activity, and aldosterone excretion 22 . These changes might increase blood pressure, and indeed such an effect has been described with HRT 23 and, perhaps more convincingly, with oral contraceptives 24 . Current oral therapies do not appear to increase blood pressure, even in hypertensive women 25, 26 .…”

Section: The Metabolic Effects Of Non‐oral Administrationmentioning

confidence: 99%

The metabolic consequences of treating postmenopausal women with non‐oral hormone replacement therapy

Crook

1997

BJOG

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Objective To define the metabolic profile of postmenopausal hormone replacement therapies when delivered through gels, patches, implants or other non-oral routes. Such information may be useful in the absence of reliable clinical data on the effects of these therapies on the risk of cardiovascular disease.Design and methods Selective literature review. Patients Postmenopausal women.Results Non-oral oestrogen therapies fail to invoke the hepatic response associated with oral therapy. Changes in hepatic protein synthesis are minimal and so plasma levels of binding globulins and other proteins tend to be normal. Many ofthe perturbations of the haemostatic system seen with oral therapy are avoided. In the absence ol' hepatic over-synthesis of apolipoproteins, plasma lipoprotein levels are unchanged or reduced. The direct effects of oestrogen on vascular function are apparent when the hormone is administered non-orally. ConclusionsThe net effect of non-oral oestrogen therapies on the risk of cardiovascular disease is difficult to predict on the basis of current data. Some changes in plasma lipoprotein levels, such as the reduced fasting levels of triglycerides, would be considered desirable, but the cardioprotective increase in levels of highdensity lipoproteins is absent. The differential effect on haemostasis markers is promising, but preliminary data relating to transdermal patches fail to support the idea that non-oral therapies will avoid the increased risk of venous thromboembolism associated with oral therapy. The ability of non-oral therapies to improve vascular function implies that they will offer postmenopausal women at least some of the cardiovascular protection seen with oral therapy.

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Section: The Metabolic Effects Of Non‐oral Administrationmentioning

confidence: 99%

The metabolic consequences of treating postmenopausal women with non‐oral hormone replacement therapy

Crook

1997

BJOG

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“…Oral contraceptives may appear to reduce the efficacy of antihypertensive therapy since it is well known that they cause an elevation of blood pressure in most patients (Weir, 1976). The rise in blood pressure is thought to be due to a rise in plasma renin activity and plasma renin substrate (Laragh et aI., 1967;Newton et aI., 1968).…”

Section: Antihypertensive Drugsmentioning

confidence: 99%

Clinical Pharmacokinetics of Oral Contraceptive Steroids

Orme

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Breckenridge

1983

Clinical Pharmacokinetics

159

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Oral contraceptive steroids are of 2 types: oestrogens, of which ethinyloestradiol is the most important, and progestagens, of which levonorgestrel and norethisterone are the most commonly used. All these steroids can be measured by a number of analytical techniques but there is little doubt that radioimmunoassay is the most convenient. All. the steroids are well absorbed in humans but while levonorgestrel is completely bioavailable, norethisterone has an average bioavailability of 70%. Ethinyloestradiol, too, is subject to presystemic metabolism with a mean bioavailability of 40 to 45%. The main site of presystemic metabolism is the gut wall, with the production of ethinyloestradiol sulphate. The progestagens norethynodrel, ethynodiol diacetate and lynoestrenol are quantitatively metabolised to norethisterone.The pharmacokinetics of the contraceptive steroids are best described by a 2-compartment open model. The terminal plasma half-life of levonorgestrel varies from 11 to 45 hours and of norethisterone from 5 to 14 hours. The Ii-phase half-life of ethinyloestradiol varies from 6 to 20 hours. The apparent volume of distribution of these contraceptive steroids (after intravenous administration) is between 1.5 and 4.3 Llkg. During long term treatment with oral contraceptive steroids, steady-state plasma concentrations of ethinyloestradiol (24 hours after administration) are between 10 and 200 pg/m!. Plasma concentrations of norethisterone and levonorgestrel at steady-state are higher than predicted from the single-dose kinetics because of enhanced binding of the progestagens following the induction of sex hormone binding globulin (SHBG) by ethinyloestradiol. Concentrations are in the range of 1.6 to 15.2 nglml for norethisterone and 0.8 to 4.5 nglml for levonorgestrel.All the contraceptive steroids are bound to proteins in plasma. Ethinyloestradiol is 97 to 98% bound to plasma albumin. The progestagens are bound both to albumin (levonorgestrel 93 to 95%; norethisterone 79 to 80%) and more specifically to SHBG. The binding capacity of SHBG can be enhanced by treatment with ethinyloestradiol or with more conventional enzyme-inducing drugs such as phenobarbitone, carbamazepine or rifampicin.Norethisterone and levonorgestrel are chiefly metabolised by reduction in the A ring and this is followed by conjugation with glucuronide or sulphate. The metabolism of levonorgestrel is stereoselective. Ethinyloestradiol is primarily hydroxylated at the 2 position but a wide variety of hydroxylated and methylated metabolites are formed and these are present both free and as glucuronide and sulphate conjugates. Ethinyloestradiol is conjugated directly at the 3 position (unlike the progestagens) and thus is liable to enterohepatic recirculation. Ethinyloestradiol sulphate concentrations in plasma are many times higher than that of the unchanged drug.

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“…While the dose of oestrogen contained in the oral contraceptive pill is relatively small, its administration has been shown to induce small rises in arterial blood pressure and retention of salt and water in most normal women (Walters & Lim 1970;Fisch et al 1974;Weir et al 1974). There is also evidence to suggest that these changes are dose-dependent (Walters & Cain 1973).…”

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confidence: 99%

Haemodynamic changes and left ventricular performance during high‐dose oestrogen administration to male transsexuals

Slater

Gude

Clarke

et al. 1986

BJOG

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Serial haemodynamic and systolic time interval measurements in 17 male transsexuals during high-dose oestrogen administration were compared with control values obtained after oestrogen withdrawal. During oestrogen treatment, cardiac output, stroke volume, plasma volume and total blood volume increased while total peripheral resistance, diastolic blood pressure and red cell mass decreased significantly. Changes in heart rate and systolic blood pressure were not significant. Despite a much higher dose of oestrogen, the haemodynamic changes observed in this study are similar in magnitude to those occurring in women taking oral contraceptives. Significant changes in systolic time intervals during oestrogen treatment were a shortened pre-ejection period (PEP) index, a prolonged left ventricular ejection time (LVET) index and a decreased PEP/LVET ratio indicating that left ventricular performance was augmented.

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Blood pressure in women taking oral contraceptives

Cited by 26 publications

References 11 publications

The metabolic consequences of treating postmenopausal women with non‐oral hormone replacement therapy

The metabolic consequences of treating postmenopausal women with non‐oral hormone replacement therapy

Clinical Pharmacokinetics of Oral Contraceptive Steroids

Haemodynamic changes and left ventricular performance during high‐dose oestrogen administration to male transsexuals

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