Combined oral contraceptives (OCs) raise the blood pressure of all women using them. In most cases the elevation is minimal, 4 mm Hg for systolic pressure and 1 mm Hg for diastolic pressure on average, but it is statistically significant and correlated with age and personal history of hypertension. In 4-5% of women the hypertensive effect is frankly pathological. The decline during the 1970s of the estrogen dose from 100 to 50 mcg reduced the hypertensive effect of OCs, but the decline from 50 to 30 mcg did not produce a parallel decline in hypertensive effect. 3 times as many OC users as women in the general population have blood pressures in excess of 160/90. The hypertensive effect of OCs was initially exclusively attributed to estrogens, but evidence has been accumulating of a hypertensive effect of at least the more estrogenic progestins, and there is also evidence that the dose is significant. The limited available data suggest that estrogen replacement therapy at menopause has the same hypertensive effect. The main cardiac risk is coronary insufficiency, which is rare in young women and only increases slightly for OC users in the absence of other vascular risk factors. Data on the effect on cardiac risks of postmenopausal estrogen therapy have been contradictory, with some suggesting that estrogen therapy results in increased rates of coronary insufficiency and others suggesting some protective effect. All studies were agreed that smoking during estrogen therapy presented a significant risk. The coronary risks could be almost eliminated if the classic contraindications of OCs were rigorously respected. Age over 35, hypertension, diabetes, and hyperlipidemia should preclude use of OCs. Natural hormones administered parenterally, such as 17-beta-estradiol and natural progesterone, do not seem to have the same secondary effects as orally administered synthetic hormones. Confirmation of their vascular innocuity will require longterm prospective studies on samples of sufficient size.