Sympathetic overactivity in pregnancy induced hypertension.

Pregnancy induced hypertension (PIH), defined as reversible hypertension beginning after the 20th gestational week, is a major cause of maternal and fetal morbidity and mortality. Although the underlying pathophysiologic mechanisms causing PIH remain enigmatic, the hypertension is not volume-dependent but rather is characterized by increased peripheral vascular resistance. To determine if increased sympathetic nerve activity (SNA) is one important mechanism mediating the increased vasomotor tone in PIH, we have measured muscle SNA (microneurography, peroneal nerve) and regional vascular resistance (plethysmography) in normotensive pregnant women (n=11) vs. those with PIH (n=6). The two groups are matched for maternal age, and all were studied after the 30th gestational week. At the time of study, mean arterial pressures, as expected, were higher in the women with PIH: 96±4 vs. 76±2 mmHg (p<.05). The major new finding is that muscle SNA was significantly higher in the women with PIH than in the normotensive pregnant women: 33±5 vs. 24±3 bursts/min. (p<.05) or 42±8 vs. 29±3 bursts/100 heart beats (p<.05). The increased SNA in the women with PIH was accompanied by increased regional vascular resistance: 45±12 vs. 24±4 units (p<.05). Thus, our results to date provide suggestive microneurographic evidence for sympathetic overactivity in pregnancy induced hypertension. Because PIH is a uniquely reversible form of human hypertension, we predict that when we restudy the same women postpartum, muscle SNA, vascular resistance and blood pressure will be comparable in both groups.