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Hypertension in pregnancy: whom and how to treat.
Author(s) -
Lubbe WF
Publication year - 1987
Publication title -
british journal of clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.216
H-Index - 146
eISSN - 1365-2125
pISSN - 0306-5251
DOI - 10.1111/j.1365-2125.1987.tb03263.x
Subject(s) - medicine , labetalol , hydralazine , atenolol , blood pressure , methyldopa , hypertension in pregnancy , nifedipine , pregnancy , pindolol , preeclampsia , essential hypertension , cardiology , anesthesia , propranolol , calcium , biology , genetics
1. Elucidation of some of the mechanisms responsible for blood pressure elevation in pregnancy has permitted therapy to be based on more rational principles. The decreased arterial reactivity encountered in normotensive pregnancy is most likely mediated by prostaglandins; preventive therapy using low dose aspirin is an option to prevent development of proteinuria in pre‐existing hypertension and provide prophylaxis against pregnancy‐induced hypertension. 2. Antihypertensive therapy utilizing sympathetic inhibition with either methyldopa or alpha‐ and beta‐adrenoceptor blockade yields the most promising results. Vasodilation with hydralazine, calcium entry blockers (nifedipine), intravenous labetalol or diazoxide is primarily used in severely hypertensive patients. The use of orally administered nifedipine in severely hypertensive women is associated with encouraging results. 3. It is clear that women with blood pressure levels greater than 170/110 mm Hg need antihypertensive therapy for maternal safety; it remains to be proven to what extent foetal growth and welfare can be improved in women with diastolic pressure levels 85‐ 110 mm Hg when adrenoceptor blocking agents are used for blood pressure control. Initial studies are suggestive of improved foetal growth, prevention of proteinuria and the respiratory distress syndrome but more long‐term controlled studies are required. 4. In a recent study, at our institution, of foetal growth during long term antihypertensive therapy, treatment with pindolol yielded better foetal growth than therapy with atenolol. It is as yet unclear whether the ISA or beta 2‐ mediated vasodilation associated with pindolol was responsible for the improved foetal growth. Further controlled studies are indicated in hypertension in pregnancy to confirm the suggested benefits of beta‐ adrenoceptor blocker therapy.

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