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  • Title: [The pathogenesis of oral contraceptive hypertension (author's transl)].
    Author: Girndt J, Scheler F.
    Journal: Klin Wochenschr; 1977 Apr 01; 55(7):347-8. PubMed ID: 870746.
    Abstract:
    Simultaneous administration of estrogen and progestogen accelerates Goldblatt-type hypertension in rats. Neither estrogen nor progestogen alone alters arterial blood pressure. In the hormonal combination the hypertensive effect of estrogen can be replaced by epsilon-amino-capronic acid and the hypertensive effect of progestogen by desoxycorticosterone acetate. Estrogen is the only substance increasing plasma renin activity. There exists no correlation between the increase of the blood pressure and the plasma renin activity in the various groups of experimental animals receiving the different hypertensive preparations. Because of this, oral contraceptive hypertension may be supposed not to result from a stimulation of the renin-angiotensin system but may easily be seen in a combination of endothelial lesions and sodium retention, the former being caused by the estrogen's effect on blood coagulation, the latter produced by the synthetic progestogen. An animal study to determine the effect of oral contraceptives on blood pressure is reported. A clamp was placed on the renal artery of a group of 18 Wistar rats to induce Goldblatt hypertension. This group and another group of 18 rats were given various dosages of ethinyl estradiol, norethisterone acetate, epslon-amino-capronic acid (as a substitute for inducing an estrogenic hypertensive effect), and/or deoxycorticosterone acetate or salt (as a substitute for induction of a gestagenic hypertensive effect). A significant increase in blood pressure was recorded only among the rats with induced Goldblatt hypertension which were administered both an estrogenic and gestagenic agent. All animals that were administered estrogen showed a significant increase in the plasma-renin activity (PRA). Animals that were administered deoxycorticosterone acetate showed a highly significant decrease in PRA.
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