[Long-term blood pressure outcome after unilateral adrenalectomy for primary hyperaldosteronism].

Objectives: To evaluate long-term results of adrenalectomy for primary aldosteronism (PA) and to identify prognostic factors associated.

Methods: Exhaustive retrospective review of all consecutive patients undergoing adrenalectomy for PA between 2002 and 2013 in our department. All patients underwent preoperative: clinical evaluation (age, sex, height, weight, systolic and diastolic BP under treatment, identification of anti-hypertension treatment), biological evaluation (potassium, renin, aldosterone) and radiological evaluation (CT and/or MRI).

[Digoxin-like natriuretic factor, raised during normal pregnancy, is increased in pregnancy-induced hypertension and pre-eclampsia].

Unlabelled: The increase of peripheral resistance in pregnancy induced hypertension (PIH) and in preeclampsia (PE) is not yet explained since previous studies have found that renin-angiotensin-aldosterone system is actually depressed, that adrenergic system is inconstantly stimulated and that vasodilating prostaglandins are inconstantly decreased. In order to get a better insight in the pathogenesis of PIH and PE, we have measured the 24 h urinary excretion of digoxin-like natriuretic factor (DLF) in 15 normotensive pregnant women (NP), in 29 women with PIH and in 6 women with PE under normal salt diet, without treatment. DLF have been measured by radio receptor binding assay.

[Pregnancy-induced hypertension and pre-eclampsia develop in spite of high circulating levels of cardionatrin].

Plasma cardionatrine was measured during pregnancy in 14 normotensive non pregnant women, 15 normotensive pregnant women, 35 pregnancy induced hypertension (PIH) and 10 preeclampsia (PE) and again 2 months after delivery in respectively 7, 15 and 7 cases together with plasma volume, PRA and plasma aldosterone. The plasma levels of cardionatrine are higher in pregnant normotensive women than in non pregnant normotensive women suggesting that pregnancy per se stimulates cardionatrine secretion. The higher levels of cardionatrine in PIH and specially in PE during pregnancy and the greater decrease of plasma cardionatrine after delivery in the hypertensive patients than in the normotensive controls exclude a deficiency of cardionatrine secretion in the pathogenesis of hypertension.