Role of angiotensin II in oral contraceptive hypertension in anesthetized rats

Stubbs, David H.; Johnson, J. A.; Ichikawa, Shûichi; Fowler, Wayne L.; Kilfoil, Jeannette; Keitzer, W. Ford

doi:10.1016/0024-3205(80)90193-9

Cited by 9 publications

(5 citation statements)

References 10 publications

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“…The infusion of [Sar',Ile 8 ]Ang II in doses sufficient to block the pressor response to infused Ang II failed to lower the arterial pressure in the hypertensive rats treated with mestranol or in those treated with mestranol plus norethynodrel; this is strong evidence that the hypertension was not simply due to the effect of elevated plasma levels of Ang II on vascular smooth muscle cells. These results are in contrast to earlier ones of Stubbs,27 who in the same laboratory did obtain a fall in pressure with another Ang II antagonist, [Sar',Ala 8 ]Ang II. Their results may have been due to pentobarbital, an anesthetic agent known to increase renin release.…”

Section: Oral Contraceptives and Elevated Blood Pressurecontrasting

confidence: 99%

“…A few investigators have had negative results, but these experiments usually involved short-term administration of the hormones. Noteworthy are the • studies of Fregley, 26 Stubbs and co-workers, 27 and Fowler and colleagues. 21 The hormones were administered in the chow for 5 to 6 months, and blood pressure was measured by carotid cannulation in addition to the tail-cuff method.…”

Section: Oral Contraceptives and Elevated Blood Pressurementioning

confidence: 99%

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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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Section: Oral Contraceptives and Elevated Blood Pressurecontrasting

confidence: 99%

Section: Oral Contraceptives and Elevated Blood Pressurementioning

confidence: 99%

Oral contraceptives and hypertension.

Woods

1988

Hypertension

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“…In a model of hypertension induced by a 26-week period of administration of mestranol and norethinodrel, infusion of the competitive angiotensin II receptor antagonist saralasin was associated with a decrease in mean arterial pressure of 28 mm Hg in anesthetized, female rats, whereas no change occurred in controls. 18 In a further larger study from the same laboratory, saralasin failed to alter arterial pressure in similarly pretreated but conscious rats, despite the finding of a markedly elevated level of plasma renin substrate (but not renin activity or renin concentration). 19 In women taking OC, the response of arterial pressure to saralasin was believed to predict the change in blood pressure observed after discontinuation of steroids.…”

Section: Discussionmentioning

confidence: 99%

Renal Characteristics and Effect of Angiotensin Suppression in Oral Contraceptive Users

et al. 1999

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Abstract-The determinants of the increase in arterial blood pressure associated with the use of estrogen-progestogen oral contraceptives (OC) remain poorly known. The purpose of this study was to assess the renal characteristics and the role of the renin-angiotensin system in women with OC-associated hypertension. Urinary clearances of technetium-labeled diethylene triaminopentaacetic acid (glomerular filtration rate) and 131 I-ortho iodohippurate (effective renal plasma flow) were estimated before and after acute administration of captopril in 38 women who became hypertensive while taking OC, 38 non-OC users with essential hypertension matched for age, body mass index, and level of blood pressure, and 38 normotensive women (19 with and 19 without OC). Plasma renin activity was higher in OC hypertensives when compared with those with essential hypertension, but captopril-induced changes in blood pressure and renal hemodynamics and function were similar in both groups. In addition, 24-hours urinary albumin excretion was increased in OC users when compared with nonusers with similar arterial blood pressure. In 13 hypertensive women followed up for 6 months after OC withdrawal, a decrease in plasma renin activity, blood pressure, and glomerular filtration rate but no significant change in urinary albumin excretion and captopril-induced changes in blood pressure and renal hemodynamics were observed. These results indicate that the use of OC is associated with an increased albuminuria and no evidence of a prominent role for the renin-angiotensin system in the maintenance of high blood pressure and renal hemodynamics when compared with non-OC users with essential hypertension. 1 OC use may also result, albeit rarely, in accelerated hypertension 2 and biopsy-proven renal damage in the absence of primary renal disease.3 When compared with earlier studies, a decreased cardiovascular morbidity was recently observed in OC users, possibly because of a tendency to refrain from OC in smoking older women and the reduction in dosages of both estrogen and progestogen components to about one fifth to one sixth.1 The absolute cardiovascular risk associated with OC use is now rather low in women with no risk factors for cardiovascular disease. 4 However, a recent worldwide survey indicated that among current OC users, a history of hypertension increased the risk of ischemic stroke by 11-fold in western Europeans and even more in subjects from developing countries. 5A small elevation in blood pressure is observed in almost all women taking OC, 6 reaching a level Ͼ140 to 90 mm Hg in 5% of those taking combined products containing Ͼ50 g estrogen. 7 In a recent large prospective cohort study conducted in American nurses, a doubling in the adjusted relative risk for hypertension was documented in current users of low-dose OC.8 Although hypertension is a fairly common side effect of OC, it is not agreed on whether the risk of OC-associated hypertension increases with the duration of OC use. 4,9 In addition, the mechanisms involved in the...

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“…β2-AR is related to inotropic action of the heart. Several studies have shown that estradiol administration induces hypertension in ovariectomized rats [18,[35][36][37][38][39]. Thus, the lower levels of β2-AR expression may reduce the inotropic action of the heart, inducing a compensatory increase in heart rate to maintain cardiac output.…”

Section: Comparison Of Heart Rate Between the C And E2 Groupsmentioning

confidence: 99%

Daily Changes of Body Temperature and Heart Rate are Modulated after Estradiol Depletion in Female Rats

Marui¹

2016

Anat Physiol

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We assessed the influence of estradiol depletion on daily changes of core temperature, spontaneous activity, and heart rate in female rats. In addition, we evaluated the effects of estradiol depletion on β-adrenoreceptors (AR) in the heart and plasma norepinephrine. Rats were bilaterally ovariectomized and two tubes that either contained estradiol (E2) or were empty (C) were placed subcutaneously in each rat's abdominal cavity. The tubes were removed 10 days later. Core temperature and heart rates were continuously measured by biotelemetry before and 1, 7, and 21 days after removal of the tubes (PRE and Days 1, 7, and 21). Core temperature was higher in the E2 group than in the C group at 2330-0130 h on PRE and on Days 1-21. Core temperature exceeded the PRE level in the E2 group at 1430-1830 h on Days 1-21. Heart rates were lower in the E2 group than the C group throughout the day on PRE and on Days 1-21. β1-AR expression and plasma norepinephrine levels were lower in the E2 group than in the C group on PRE. Heart rates in the E2 group exceeded the PRE level on Days 1-21. We concluded that the depletion of plasma estradiol modulates daily changes of core temperature and heart rate, an effect that occurs immediately after the estradiol depletion. In addition, plasma norepinephrine and β-AR in the heart may at least partially affect heart rate. A n a to my & P h y s io logy: C u r r e n t Re sea rc h

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Role of angiotensin II in oral contraceptive hypertension in anesthetized rats

Cited by 9 publications

References 10 publications

Oral contraceptives and hypertension.

Oral contraceptives and hypertension.

Renal Characteristics and Effect of Angiotensin Suppression in Oral Contraceptive Users

Daily Changes of Body Temperature and Heart Rate are Modulated after Estradiol Depletion in Female Rats

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