Relation between resting sympathetic outflow and vasoconstrictor responses to sympathetic nerve bursts: sex differences in healthy young adults

Abstract

Previous studies have demonstrated an inverse relation between resting muscle sympathetic nerve activity (MSNA) and vasoconstrictor responsiveness (i.e., sympathetic transduction), such that those with high resting MSNA have low vascular responsiveness, and vice versa. The purpose of this investigation was to determine whether biological sex influences the balance between resting MSNA and beat-to-beat sympathetic transduction. We measured blood pressure (BP) and MSNA during supine rest in 54 healthy young adults (27 females: 23 ± 4 yr, 107 ± 8/63 ± 8 mmHg; 27 males: 25 ± 3 yr, 115 ± 11/64 ± 7 mmHg; means ± SD). We quantified beat-to-beat fluctuations in mean arterial pressure (MAP, mmHg) and limb vascular conductance (LVC, %) for 10 cardiac cycles after each MSNA burst using signal averaging, an index of sympathetic vascular transduction. In females, there was no correlation between resting MSNA (burst incidence; burst/100 heartbeats) and peak ΔMAP ( r = −0.10, P = 0.62) or peak ΔLVC ( r = −0.12, P = 0.63). In males, MSNA was related to peak ΔMAP ( r = −0.50, P = 0.01) and peak ΔLVC ( r = 0.49, P = 0.03); those with higher resting MSNA had blunted increases in MAP and reductions in LVC in response to a burst of MSNA. In a sub-analysis, we performed a median split between high- versus low-MSNA status on ΔMAP and ΔLVC within each sex and found that only males demonstrated a significant difference in ΔMAP and ΔLVC between high- versus low-MSNA groups. These findings support an inverse relation between resting MSNA and sympathetic vascular transduction in males only and advance our understanding on the influence of biological sex on sympathetic nervous system-mediated alterations in beat-to-beat BP regulation.

Sex difference in sympathetic nervous system activity and blood pressure in hypertensive patients

“…Interestingly, we found that an association between SNS activity and BP was notable in hypertensive men rather than in hypertensive women. Sex differences in SNS activity and BP had been reported in different populations 22,23 . One study conducted in 54 healthy young adults showed that resting MSNA was related to changes in mean arterial pressure in men but not women 22 .…”

“…22,23 One study conducted in 54 healthy young adults showed that resting MSNA was related to changes in mean arterial pressure in men but not women. 22 Another study compared changes in MSNA and cardiovascular variables during leg cycle exercise, with increased inspiratory muscle resistance, in seven men and eight women. During the leg cycle exercise with inspiratory resistive breathing, MSNA burst frequency increased, accompanied by an increase in mean arterial pressure in both men and women.…”

Hydration Status and Cardiovascular Function

“…Together, the conflicting results in the literature regarding the influence of Ang II and AVP on BP regulation during hypohydration suggests more investigation in this area is necessary. Finally, several studies that have been conducted regarding the influence of biological sex [189,190,191,192,193,194,195,196,197,198] and sex hormone fluctuations during the menstrual cycle in female adults [189,191,192,193,194,195,196,197] and BP regulation. These studies have provided important insight concerning the influence of sex and menstrual cycle-induced changes in blood volume on BP regulation, which is a prerequisite to studying the additional influence of hypohydration.…”

Signal-averaged resting sympathetic transduction of blood pressure: is it time to account for prevailing muscle sympathetic burst frequency?

“…regional vascular conductance). In particular, a number of recent studies have employed signal-averaging methods (4)(5)(6)(7)(8)(9)(10)(11), whereby the effects of each MSNA burst (or non-burst cardiac cycles) on hemodynamic variables (e.g. blood pressure [BP]) are tracked for 10-15 subsequent cardiac cycles (termed resting sympathetic transduction of BP).…”

“…This is an important consideration given that 1) current analyses of sympathetic transduction of BP and the sympathetic transduction slope fail to integrate the prevailing level of resting MSNA, and 2) the majority of evidence has observed a negative association between the neural stimulus and transduction response, such that sympathetic transduction of BP and the sympathetic transduction slope are lower in individuals with high resting MSNA burst frequency (4, 6-8, 11, 12). The majority of work has ascribed this negative relationship as a compensatory change to help maintain normal BP (4,(6)(7)(8)11). However, high resting MSNA burst frequency has also been described as a limitation towards quantifying resting sympathetic transduction of BP (12, 21) and thought to prevent its use in individuals with high resting MSNA (3,21,22).…”