Regulation of Sympathetic Nerve Activity During the Cold Pressor Test in Normotensive Pregnant and Nonpregnant Women

Baseline neurovascular transduction is reduced in normotensive pregnancy; however, little is known about changes to neurovascular transduction during periods of heightened sympathetic activation. We tested the hypothesis that, despite an exacerbated muscle sympathetic nerve activity (microneurography) response to cold pressor stimulation, the blunting of neurovascular transduction in normotensive pregnant women would result in similar changes in vascular resistance and mean arterial pressure (Finometer) relative to nonpregnant controls. Baseline neurovascular transduction was reduced in pregnant women relative to controls when expressed as the quotient of both total resistance and mean arterial pressure and sympathetic burst frequency (0.32 +/- 0.07 versus 0.58 +/- 0.16 mmHg/L/min/bursts/min, P<0.001 and 2.4 +/- 0.7 versus 3.6 +/- 0.8 mmHg/bursts/min, P=0.001). Sympathetic activation was greater across all 3 minutes of cold pressor stimulation in the pregnant women relative to the nonpregnant controls. Peak sympathoexcitation was also greater in pregnant than in nonpregnant women, whether expressed as sympathetic burst frequency (+17 +/- 13 versus +7 +/- 8 bursts/min, P=0.049), burst incidence (+17 +/- 9 versus +6 +/- 11 bursts/100 hb, P=0.03), or total activity (+950 +/- 660 versus +363 +/- 414 arbitrary units, P=0.04). However, neurovascular transduction during peak cold pressor-induced sympathoexcitation remained blunted in pregnant women (0.25 +/- 0.11 versus 0.45 +/- 0.08 mmHg/L/min/bursts/min, P<0.001 and 1.9 +/- 1.0 versus 3.2 +/- 0.9 mmHg/bursts/min, P=0.006). Therefore, mean arterial pressure (93 +/- 21 versus 99 +/- 6 mmHg, P=0.4) and total peripheral resistance (12 +/- 3 versus 14 +/- 3 mmHg/L/min) were not different between pregnant and nonpregnant women during peak sympathoexcitation. These data indicate that the third trimester of normotensive pregnancy is associated with reductions in neurovascular transduction, which result in the dissociation of sympathetic outflow from hemodynamic outcomes, even during cold pressor-induced sympathoexcitation.