The impact of oral contraceptive pill use on sympathetic transduction at rest in young females.

Abstract

Although previous work has demonstrated that oral contraceptive pill (OCP) use does not affect resting muscle sympathetic nerve activity (MSNA), growing evidence indicates that it attenuates neurogenic vasoconstriction. Despite these advances, it remains unknown how OCP use affects the ability of MSNA to dynamically control vascular tone and arterial blood pressure (BP) on a beat-by-beat basis. Thus, we tested the hypothesis that, compared with naturally menstruating females (MC), those using OCPs will exhibit attenuated sympathetic vascular transduction at rest. Forty-three females [MC: n = 21, 26 (4) yrs; OCP: n = 22, 24 (4) yrs; data are presented as means (SD)] completed 10 min of supine rest with continuous measurements of beat-by-beat BP, femoral artery blood flow (26 females; MC: n = 13, OCP: n = 13), and MSNA. Spike-triggered averaging was used to determine sympathetic transduction into leg vascular conductance (LVC) and BP for 12 cardiac cycles following MSNA bursts. Overall sympathetic-BP transduction (P = 0.293), as well as sympathetic-BP transduction of MSNA burst quartiles (P = 0.741) and burst firing patterns (P = 0.452) were not different between the MC and OCP groups. Conversely, sympathetic vascular transduction per unit MSNA burst amplitude (P = 0.026) and burst firing pattern (P = 0.014) were attenuated among females using OCPs. In addition, females using OCPs demonstrated progressively smaller leg vasoconstrictor responses as a function of MSNA burst firing pattern compared with MC females (P = 0.021). Collectively, these data indicate that, in premenopausal females, OCP use attenuates the leg vasoconstrictor responses to bursts of MSNA, particularly during periods of increased sympathetic neural drive, without affecting the transduction of MSNA bursts into beat-by-beat changes in BP.NEW & NOTEWORTHY This study investigated the impact of OCP use on the transduction of MSNA bursts into regional vasoconstriction and blood pressure in premenopausal females. We demonstrated that females using OCPs exhibit attenuated sympathetic transduction into LVC; however, this does not translate to reductions in sympathetic blood pressure transduction. Collectively, these data indicate that OCP use may alter the local vasoconstrictor response to bursts of MSNA; however, compensatory mechanisms may contribute to maintain sympathetic blood pressure transduction.