Hypertension in pregnancy: a physiological response to a pathological problem?
In pregnancy-induced hypertension the secondary wave of trophoblast invasion fails, there is a progressive increase in pressor responsiveness to angiotensin II and an imbalance develops in the prostacyclin:thromboxane ratio towards thromboxane. As pregnancy progresses one can imagine that fetal demands gradually outstrip the ability of the relatively narrowed spiral arteries to perfuse the placenta. By analogy with renal artery stenosis, a defence mechanism would be stimulated (synthesis both of renin and vasodilator prostanoids) with systemic hypertension but improved perfusion. Where vasodilator synthesis is impaired, hypertension alone, with worsening perfusion, would ensue.
Broughton Pipkin
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Department of Obstetrics and Gynaecology, Queen's Medical Centre, Nottingham, England.
D000328:Adult; D005260:Female; D006801:Humans; D006973:Hypertension / Q000150:complications* / Q000503:physiopathology; D011247:Pregnancy; D011249:Pregnancy Complications, Cardiovascular / Q000503:physiopathology*