Twentysix women with pregnancy-induced hypertension have been randomly treated with either labetalol or Aldomet. A more satisfactory control of blood pressure was obtained with labetalol with minimal side-effects. After two weeks of treatment with labetalol renal function had significantly improved with a markedly lower incidence of proteinuria. More patients went into spontaneous labour following labetalol than following Aldomet; the Bishop score was also higher in this group. No adverse effects attributable to labetalol were noted in the baby either ante- or post-natally.

1 Nineteen pregnant patients whose mean arterial pressure (MAP) was persistently greater than or equal to 103.3 mmHg were given labetalol or methyldopa. 2 Singificant falls (P less than 0.001) in BP only occurred in the group treated with labetalol, and daily BP control was better in this group. 3 Two severely hypertensive patients were successfully treated with intravenous labetalol. 4 There was a higher incidence of spontaneous labour in the labetalol group and a significant difference (P less than 0.05) in the Bishop score of the cervix between the two groups. 5 There were no apparent detrimental effects on the foetus antenatally, during labour or post partum. 6 Slight breathlessness in one patient treated with labetalol was the only side‐effect observed but drowsiness, headache and postural hypotension were reported in patients receiving methyldopa.

Summary. Plasma renin activity, plasma renin concentration, plasma renin substrate, plasma angiotensin II and plasma aldosterone were measured in 10 true primiparae, normotensive throughout pregnancy, for 4 days after a spontaneous vaginal delivery. The concentration of all the measured variables, except plasma renin substrate, fell steeply over the first 3 days post partum. In four of the 10 patients, all components of the renin‐angiotensin system increased in concentration somewhat thereafter, although not to the levels of the first day post partum. There are multiple potential sources of renin in the fetoplacental unit and it is possible that this‘pregnancy’ renin may be capable of the partial suppression of the maternal renin production during pregnancy. The slight rebound observed in some patients may represent a hunting for re‐establishment of non‐pregnant values.

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