Oral contraceptives and hypertension.

Abstract

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.

Transdermal oestrogen reduces daytime blood pressure in hypertensive women

“…21 Oestrogen also elicits an effect on prostacyclin production which also has a vasodilating potential. 22 It is well known that oestrogen influences the renin-angiotensin system, 23 but acute antihypertensive effects via this system have not been well documented. The difference in BP response seen with the oestrogens available in oral contraceptives compared to oestrogens used during HRT could be explained by differences in doses, types and administration of the oestrogen used, but also by the fact that an influence on the renin-angiotensin system can be dual with vasodilation by pro-renin, and vasoconstriction by renin.…”

Hypertension in women

“…This effect may be related to the calcium antagonist effects of oestrogen 49 or an Reports on the effect of OCs on hypertension are mixed and difficult to compare for a number of reasons: many studies included few subjects and lacked appropriate controls; OC preparations changed over time, and differing combinations of oestrogen and progestogen which may act synergistically or antagonistically. 54 Following Woods' initial report 55 in 1967 of elevated blood pressure in hypertensive women on OCs, several investigators documented the considerable lowering of blood pressure among hypertensive women upon stopping OCs. [56][57][58][59][60] Laragh and Sealey 56 reported elevations in renin substrate concentration and aldosterone excretion, as well as abnormalities in renin activity and renin reactivity in women on OC therapy.…”

Use of oral contraceptives and serum beta-carotene

“…In our study, a considerable percentage of OC users were also smokers, thus increasing the risk of low beta-carotene levels and the subsequent possible negative effects on health. The strong association between OC use and beta carotene in women above 35 y of age who already have a substantial risk of cardiovascular diseases (Woods, 1988) strengthens the possibility that OC use has a relevant negative impact on health by decreasing beta-carotene levels.…”