T he risk of developing cardiovascular disease is lower in young women when compared with similarly aged men. [1][2][3] However, pregnancy represents a period of increased susceptibility to disordered cardiovascular regulation for women. Pregnant women have an elevated risk for orthostatic intolerance. 4,5 Moreover, ≤8% of pregnancies are associated with the development of de novo hypertension. 6 The cause of such hypertensive pregnancy disorders remains unclear, and as a result, there exist few approaches by which clinicians can predict, screen, or treat the development of the hypertensive disorders of pregnancy (gestational hypertension and preeclampsia). Previous data have shown that the vascular response to the cold pressor test (CPT) is blunted in normal pregnant women compared with women in the nonpregnant, postpartum state. 8 However, an elevated pressor response to the CPT has been observed in women with 9 or who subsequently develop 10 preeclampsia. As such, the CPT has been suggested as a simple screening tool for pregnancy-related hypertensive disorders. The mechanisms driving these divergent responses remain unknown; however, sympathetic nervous system activity is a primary determinant of the pressor response to the CPT.
11Differing vascular responses to the CPT may be mediated by altered sympathetic responses or altered translation of sympathetic activity into a vascular outcome (neurovascular transduction). Studies conducted over the past 2 decades have indicated, albeit not universally, 12 that normotensive Abstract-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.