To measure high-sensitivity C-reactive protein (hsCRP) levels and to assess the presence of metabolic syndrome (MS) after puerperium in women diagnosed with various hypertensive disorders during pregnancy (HDP), a consecutive, cross-sectional case study at the 15th week after gestation. The sample consisted of 264 women who were admitted to a women's hospital. The diagnoses consisted of transient gestational hypertension (TGH¼43.2%), preeclampsia (PC¼29.5%), chronic hypertension (CH¼20.1%) and PC superimposed on CH (7.2%). A diagnosis of previous hypertension was present in 45.8% of the CH group. The prevalence of MS was 16.7% (CH¼42.1%, TGH¼13.9%, PC¼4.1%, Po0.001). The average hsCRP levels for the CH, TGH and PC groups were 3.79±2.76, 3.55±3.15 and 2.89±3.02, respectively (P¼0.040). The levels of hsCRP were higher in women with MS (4.71±3.15 vs. 3.01±2.88 mg l À1 in those without MS, Po0.001), and they increased when a higher number of MS criteria was fulfilled (Po0.001). The results demonstrated a positive correlation between hsCRP levels and body mass index (BMI) (r¼0.46), waist circumference (r¼0.50) or the number of fulfilled MS criteria (r¼0.56). The results suggest differences in vascular risk that depend on the type of HDP and on the prevalence of MS. The prevalence of MS was notably higher in the CH group, intermediate among the TGH group and much lower in the PC group. Differences in hsCRP levels also depended on the type of HDP (higher levels in CH and TGH patients in comparison with PC patients). Women with MS had higher hsCRP levels compared with women without MS, and the levels correlated with the number of MS criteria fulfilled. This result suggests that subclinical inflammatory status is correlated with the number of MS components present. Furthermore, hsCRP levels increased with increasing BMIs and waist circumferences.

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In essential hypertensive patients "exaggerated natriuresis" is a response to acute volume expansion. However, the underlying mechanisms for this remain to be determined. We studied 19 patients with essential hypertension (HP) and 9 normotensive subjects (NS). In all examined subjects the response to acute central volume expansion, without the plasma compositional change that Trendelenburg's position involves, was evaluated during 90 min (period T) after a similar period of deambulation (period D). Mean blood pressure (MBP), tubular sodium handling by the lithium clearance technique, plasma renin activity (PRA), plasma aldosterone (PA), plasma catecholamines and urine prostaglandine E2 and kallikrein were assessed after D and T. MBP was significantly higher in HP than in NS (p = 0.00001). HP showed "exaggerated natriuresis" after T (fractional excretion of sodium increased from 0.55 +/- 0.1% after D to 1.20 +/- 0.2% after T, p < 0.01). This was because of a decrease in their proximal fractional reabsorption of sodium (from 74.96 +/- 1.8% after D to 62.50 +/- 2.8% after T, p < 0.01). Plasma epinephrine and plasma dopamine after T were significantly lower than in standing position in HP (p < 0.01) but no in NS. The decrease in plasma renin activity after T in HP was 53%, and 32% in NS. There were not any significant differences between groups in the other neurohormonal systems studied. We conclude that the major determinant of "exaggerated natriuresis" in hypertensive patients is a higher stimulation of the cardiopulmonary receptors following Trendelenburg's position and consequently stronger reflex inhibition of sympathetic system activity and renin-angiotensin II activity. The "exaggerated natriuresis" after Trendelenburg's position in HP was an expression of abnormal pressure natriuresis.