scholarly journals Role of the ovarian cycle on neural cardiovascular control in sleep-deprived women

2015 ◽  
Vol 118 (4) ◽  
pp. 419-426
Author(s):  
Huan Yang ◽  
John J. Durocher ◽  
Robert A. Larson ◽  
Jason R. Carter

The midluteal (ML) phase of the ovarian cycle is often sympathoexcitatory compared with the early follicular (EF) phase. We recently reported that 24-h total sleep deprivation (TSD) augmented cardiovascular reactivity in both men and women, but that sex differences existed in resting muscle sympathetic nerve activity (MSNA) responses to TSD. In the present study, we hypothesized increased resting MSNA and augmented cardiovascular reactivity to acute laboratory stressors during the ML phase in sleep-deprived women. Heart rate (HR), mean arterial pressure (MAP), forearm vascular conductance (FVC), and MSNA were measured in 14 eumenorrheic women (age, 20 ± 1 yr) during 10 min supine rest, 5 min mental stress (MS) trial, and 2 min cold pressor test (CPT) trial. Subjects were tested twice after TSD: once during EF phase and once during ML phase (randomized, crossover design). Estradiol (29 ± 2 vs. 63 ± 8 pg/ml, P = 0.001) and progesterone (1.6 ± 0.2 vs. 4.4 ± 0.7 ng/ml, P = 0.002) were elevated during the ML phase. Resting supine MAP (75 ± 2 vs. 72 ± 1 mmHg, P = 0.042) was lower during the ML phase. In contrast, resting supine HR, MSNA, and FVC were not significantly different between EF and ML phases. MAP, HR and FVC reactivity to MS were not statistically different between the EF and ML phases. Similarly, MAP and HR reactivity to CPT were not different between the ovarian phases. Contrary to our original hypothesis, the ML phase was not associated with sympathoexcitation or exaggerated cardiovascular reactivity in sleep-deprived premenopausal women. However, our data reveal elevated resting blood pressure during the EF phase in sleep-deprived women.

2012 ◽  
Vol 113 (6) ◽  
pp. 903-908 ◽  
Author(s):  
Huan Yang ◽  
John J. Durocher ◽  
Robert A. Larson ◽  
Joseph P. DellaValla ◽  
Jason R. Carter

Exaggerated cardiovascular reactivity to mental stress (MS) and cold pressor test (CPT) has been linked to increased risk of cardiovascular disease. Recent epidemiological studies identify sleep deprivation as an important risk factor for hypertension, yet the relations between sleep deprivation and cardiovascular reactivity remain equivocal. We hypothesized that 24-h total sleep deprivation (TSD) would augment cardiovascular reactivity to MS and CPT and blunt the MS-induced forearm vasodilation. Because the associations between TSD and hypertension appear to be stronger in women, a secondary aim was to probe for sex differences. Mean arterial pressure (MAP), heart rate (HR), and muscle sympathetic nerve activity (MSNA) were recorded during MS and CPT in 28 young, healthy subjects (14 men and 14 women) after normal sleep (NS) and 24-h TSD (randomized, crossover design). Forearm vascular conductance (FVC) was recorded during MS. MAP, FVC, and MSNA ( n = 10) responses to MS were not different between NS and TSD (condition × time, P > 0.05). Likewise, MAP and MSNA ( n = 6) responses to CPT were not different between NS and TSD (condition × time, P > 0.05). In contrast, increases in HR during both MS and CPT were augmented after TSD (condition × time, P ≤ 0.05), and these augmented HR responses persisted during both recoveries. When analyzed for sex differences, cardiovascular reactivity to MS and CPT was not different between sexes (condition × time × sex, P > 0.05). We conclude that TSD does not significantly alter MAP, MSNA, or forearm vascular responses to MS and CPT. The augmented tachycardia responses during and after both acute stressors provide new insight regarding the emerging links among sleep deprivation, stress, and cardiovascular risk.


Author(s):  
Guillaume Lamotte ◽  
Christopher J. Boes ◽  
Phillip A. Low ◽  
Elizabeth A. Coon

Author(s):  
Ryosuke Takeda ◽  
Abigail S.L. Stickford ◽  
Stuart A. Best ◽  
Jeung-Ki Yoo ◽  
Yu-Lun Liu ◽  
...  

Excessive salt intake is considered a risk factor for the development of hypertension. Additionally, aberrant neuro-circulatory responses to a cold stimulus are associated with an increased risk of hypertension. This study aimed to determine whether salt loading versus salt reduction would impact hemodynamic and sympathetic neural responses during the cold pressor test (CPT) in premenopausal women with a history of normal pregnancy. Nine healthy premenopausal women [42±3 (SD) yr] were given a standardized isocaloric high salt (HS; 250 mEq sodium/day) or low salt (LS; 50 mEq sodium/day) diet for 1-week each (~2 months apart with the order randomized), while water intake was ad libitum. Laboratory testing was performed following each HS and LS period in the mid-luteal phase of the menstrual cycle. Subjects were in the supine position and beat-by-beat blood pressure (BP), heart rate (HR) and muscle sympathetic nerve activity (MSNA) were continuously measured during 1-minute baseline followed by 2-minute CPT and 3-minute recovery. BP and HR increased during the CPT (both P<0.001); the responses were similar between HS and LS. MSNA increased during the CPT, but the increment (D) was greater during HS than LS (29±6 vs. 15±4 bursts/min; P<0.001). The transduction of MSNA for vasoconstriction during the CPT was lower in HS (P<0.05). Thus, salt loading augments sympathetic neural reactivity to the cold stimulus with similar pressor responses compared to salt reduction, which may be attributed to the blunted neurovascular transduction ─ a compensatory mechanism for hemodynamic homeostasis in premenopausal women with a history of normal pregnancy.


1995 ◽  
Vol 269 (2) ◽  
pp. R406-R412 ◽  
Author(s):  
J. S. Floras

I have previously documented an inhibitory effect of atrial natriuretic factor (ANF) on postganglionic muscle sympathetic nerve activity (MSNA) in normal subjects that was consistent with either a central or ganglionic sympathoinhibitory action. To test the latter hypothesis, I examined, in seven young normotensive men, the effect of saline (as vehicle) and ANF (50 micrograms, then 50 ng.kg-1.min-1), given on 2 separate days according to a random double-blind study design, on blood pressure, heart rate, and MSNA before and after ganglionic neurotransmission was stimulated with edrophonium (ED; 12 mg iv), a rapidly reversible acetylcholinesterase inhibitor without central nervous system effects, and during subsequent augmentation of central sympathetic outflow by a cold pressor test (CPT). In five of these subjects, the protocol was replicated during nitroprusside infusion (0.4 micrograms.kg-1.min-1). ED increased MSNA during vehicle (P < 0.005) and nitroprusside (P < 0.003) but not during ANF infusion. The sympathoneural response to the combined stimuli of ED and CPT was also attenuated by ANF compared with either saline or nitroprusside infusions. Conclusions were that 1) postganglionic MSNA is increased by ED, 2) this facilitative effect of ED is attenuated by ANF, and 3) modulation of ganglionic neurotransmission is one mechanism for the relative sympatho-inhibition observed when ANF is infused at this dose.


2009 ◽  
Vol 297 (2) ◽  
pp. H564-H568 ◽  
Author(s):  
Jeanie Park ◽  
Holly R. Middlekauff

Smoking increases cardiovascular risk in young women and eliminates the protective effect of the premenopausal state. Increased sympathetic nervous system (SNS) activity is associated with increased cardiovascular risk. One potential mechanism by which smoking increases risk is through chronic SNS activation. It has been reported that premenopausal women have high SNS activity during the midluteal (ML) phase, which falls to low levels during the early follicular (EF) phase. We tested the hypothesis that smoking disrupts this fall in SNS activity during the EF phase. We measured blood pressure and muscle sympathetic nerve activity (MSNA) using microneurography in 11 premenopausal female smokers and 11 age-matched nonsmoking controls at two separate times during the ovarian cycle: ML phase (8–10 days after the luteinizing hormone surge) and EF phase ( days 1–4 of the menstrual cycle). The change in MSNA from the EF phase to the ML phase was significantly different between the smoking and nonsmoking groups ( P = 0.036). Whereas there was a significant decrease in MSNA from the ML phase to the EF phase among nonsmoking controls (22.7 ± 3.3 vs. 17.9 ± 2.8 bursts/min, P = 0.012), MSNA remained elevated during the EF phase in smokers (22.5 ± 3.8 vs. 26.8 ± 4.0 bursts/min, P = 0.28). Surprisingly, mean arterial pressure (MAP) was significantly lower during the ML phase than in the EF phase in both nonsmokers ( P = 0.0080) and smokers ( P = 0.0094). We conclude that smoking disrupts the ovarian pattern of SNS activity by preventing the normal fall in MSNA during the EF phase of the ovarian cycle. Such chronic alterations may contribute to the pathogenesis of cardiovascular risk in young smoking females.


2020 ◽  
Vol 318 (5) ◽  
pp. H1198-H1207 ◽  
Author(s):  
Jeung-Ki Yoo ◽  
Mark B. Badrov ◽  
Mu Huang ◽  
Ryan A. Bain ◽  
Raymond P. Dorn ◽  
...  

The novel findings of the present study are that women with posttraumatic stress disorder (PTSD) have an augmented pressor response to the sympathoexcitatory stimulus of a cold pressor test (CPT) compared with healthy control subjects. Although integrated muscle sympathetic nerve activity burst responses were not significantly different between groups, total sympathetic action potential discharge in response to the CPT was markedly elevated in women with PTSD exhibiting increased firing of low-threshold axons as well as the recruitment of latent subpopulations of larger-sized axons that are otherwise silent at baseline. Aberrant autonomic circulatory control in response to sympathoexcitatory stimulus may in part explain the propensity toward developing hypertension and cardiovascular disease in this population.


Hypertension ◽  
1987 ◽  
Vol 9 (5) ◽  
pp. 429-436 ◽  
Author(s):  
R G Victor ◽  
W N Leimbach ◽  
D R Seals ◽  
B G Wallin ◽  
A L Mark

1983 ◽  
Vol 17 (4) ◽  
pp. 189-191 ◽  
Author(s):  
M. F CUMMINGS ◽  
P. M STEELE ◽  
L. J M MAHAR ◽  
D. B FREWIN ◽  
W J. RUSSELL

2002 ◽  
Vol 34 (5) ◽  
pp. S112
Author(s):  
V Bond ◽  
P Vaccaro ◽  
R Blakely ◽  
D Williams ◽  
T O. Obisesan ◽  
...  

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