Citations

A history of preeclampsia (PE) places women at higher risk for future cardiovascular disease and cognitive decline. We have previously shown that postmenopausal women with a history of PE demonstrated a reduced cerebral blood flow response to hypercapnia compared with postmenopausal women with a history of a normotensive pregnancy (NP). These findings suggest cerebrovascular effects of PE 30+ years postpartum. In addition, we have reported that women with a history of PE did not have an exaggerated pressor response to a sympathoexcitatory stimulus. However, it is possible that women with a history of PE may have an altered cerebral blood flow response to a sympathoexcitatory stimulus. In this study, middle cerebral artery blood velocity (MCAv) and beat‐to‐beat mean arterial blood pressure (MAP) were measured during isometric handgrip to fatigue (IHG) at 30% of maximal voluntary contraction followed by post‐exercise ischemia (PEI) for 90 seconds and a two minute recovery period (REC). Participants were postmenopausal women with a history of PE (n = 21; age at study = 58±5 y; years since last pregnancy = 35±3 y) and NP (n = 27; age at study = 58±5 y; years since last pregnancy = 35±3 y). Baseline MAP and MAP responses to IHG and PEI were similar between groups (p>0.05). PE women demonstrated lower MCAv at baseline (NP: 72±3 cm/s vs. PE: 57±4 cm/s), IHG (NP: 78±4 cm/s vs. PE: 63±4 cm/s), PEI (NP: 74±4 cm/s vs. PE: 60±4 cm/s), and REC (NP: 70±3 cm/s vs. PE: 58±4 cm/s) compared with NP women (p<0.05 for all). MCAv, when calculated as a percent change from baseline, was elevated during IHG in both PE and NP women as expected (p<0.05); however, PE women had an augmented MCAv response during the last third of IHG compared with NP women (NP: 9±2 % vs. PE: 13±2 %; p<0.05). PE women also had a higher MCAv response during REC compared with NP women (NP:−2±2% vs. PE: 3±2%; p<0.05). Importantly, these elevated MCAv responses occurred despite the fact that MAP was not different between groups. In summary, PE women demonstrated a lower basal cerebral blood velocity but an elevated cerebrovascular response to a sympathoexcitatory stimulus compared with NP women. This suggests that in postmenopausal women, there is an effect of pregnancy history on the sensitivity of the cerebral blood flow response to a sympathoexcitatory stimulus. Support or Funding Information NIH: AG 044170. This investigation was supported by the National Institutes of Health, under Ruth L. Kirschstein National Research Service Award T32 HL 007936 from the National Heart Lung and Blood Institute to the University of Wisconsin‐Madison Cardiovascular Research Center. This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .

Acute exercise appears to have positive influence on arterial function during the recovery period, yet the effect of obesity is poorly understood in recovery. We examined the effects of an acute bout of exercise on arterial function in obese versus healthy weight individuals. Young (23 yr), lean (n=38, BMI=22.3 kg/m 2 ) and obese (n=20, BMI=34.0 kg/m 2 ) individuals had arterial measurements obtained at rest, and 15 and 30 min following a maximal bout of aerobic exercise. Arterial tonometry and ultrasound were used to obtain central BP, arterial compliance and stiffness (beta stiffness, elastic modulus (Ep), and central pulse wave velocity (PWV)). Despite similar central mean BP, the obese group had higher cPWV following exercise. Beta stiffness and Ep responded similarly to exercise between groups. Arterial compliance was higher in obese but the response in recovery was similar between groups. Lean Obese Pre 15‐min post 30‐min post Pre 15‐min post 30‐min post Mean aortic BP 82 83 82 87 86 87 Central PWV 5.67 5.46 5.35 5.84 6.11 6.16 Beta Stiffness 5.89 6.34 5.78 4.88 6.04 5.31 Elastic Modulus 69 75 67 67 78 66 In this young cohort, obesity was associated with increased central arterial stiffness, independent of BP, but higher arterial compliance. This suggests that measures of arterial stiffness provide differential information potentially associated with where in the arterial tree measures were made.

Hypertensive pregnancy (HP) is considered a risk factor for cardiovascular disease. Blood pressure (BP) response to physical stressor is an independent marker of cardiovascular risk. However, there is limited data regarding the pressor response to acute physical stress in women with a history of HP. Hence, the aim of the study was to compare BP responses in women with a history of HP to age and parity matched controls. Beat to beat BP was recorded in postmenopausal women (age = 59 ± 1 yrs, BMI = 31 ± 2 kg/m2) with and without a history of HP at baseline and during isometric handgrip (HG) exercise (30% of MVC) to fatigue. Isometric handgrip exercise was followed by 90 seconds of supra‐systolic cuff occlusion on the exercising arm. In both groups combined (N=31), systolic blood pressure (SBP) increased significantly from baseline to HG to cuff inflation (143 ± 3 to 161 ± 3 to 167 ± 4 mmHg). Similarly, mean arterial pressure (MAP) increased significantly from baseline to HG to cuff inflation (106 ± 2 to 119 ± 2 to 122 ± 2 mmHg). Diastolic pressure (DBP) increased significantly only from baseline to HG (80 ± 1 to 88 ± 1 mmHg) and baseline to cuff inflation (89 ± 2 mmHg). However, there were no significant differences in SBP, DBP and MAP between women with and without a history of HP (p>0.05). Even though both groups had an increase in BP variables in response to HG and cuff occlusion, there was no difference in the BP response to acute physical stressors in women with a history of HP as compared to control participants. Funding: National Institute of Aging 1P50AG044170‐01 and CTSA UL1 TR000135 and HL 118154 (JNB)

<a name=“OLE_LINK2”></a><a name=“OLE_LINK1”>Hypertensive pregnancy (HP) disorders have been linked to a four‐fold increased risk for development of future cardiovascular diseases. We examined whether history of HP in postmenopausal women (N=20, 59±5 yr) influenced the risk factors for cardiovascular disease as assessed by aortic pulse wave characteristics, compared to age and parity matched controls (N=18, 60±4 yr). Non‐invasive aortic pressure waveforms were synthesized from high‐fidelity pressure waveforms obtained from SphygmoCor applanation tonometry using the radial artery. Aortic systolic and diastolic blood pressure (ASBP, ADBP), aortic augmentation index (AI x ), augmented pressure (AP), aortic pulse pressure (APP), and left ventricular wasted energy (E w ) were calculated from the generated aortic pressure waveform. There were no differences in ASBP (125±4 vs. 129±4 mmHg), ADBP (79±2 vs. 81±2 mmHg), AP (17±2 vs. 17±2 mmHg), AI x (35±2 vs. 29±1%), AI x @75BPM (31±2 vs. 29±1%), E w (3313±338 vs. 3364±432 dynes/cm 2 /s), between women with a history of HP vs. matched controls, respectively (P>0.05 for all). Body mass index was significantly higher in women with a history of HP (30.6±1 vs. 26.7±1 kg/m 2 , P<0.05), however it did not statistically influence any of the indices (P>0.05 for all). Our results suggest that postmenopausal women with a history of HP do not demonstrate elevated aortic blood pressure or altered aortic pulse wave characteristics in comparison to matched controls. </a> Supported by: National Institute of Aging 1P50AG044170‐01 and CTSA UL1 TR000135 and HL 118154

Introduction Acute estrogen infusion augments β 2 ‐adrenergic receptor responsiveness in premenopausal women. This suggests an influential role of estrogen in controlling the vasodilator responsiveness via β 2 ‐adrenergic receptors in premenopausal women. Postmenopausal women present with a reduced β 2 ‐adrenergic receptor responsiveness as compared to premenopausal women. This divergent finding in β 2 ‐adrenergic receptor responsiveness could be due to loss of endogenous estrogen postmenopause. Objective Hence, the objective of the study was to compare the β 2 ‐adrenergic vasodilator responses with and without estrogen in postmenopausal women. We hypothesized that the vasodilator effects during endothelial dependent, independent and during β 2 ‐adrenergic agonist infusion would be significantly greater with acute, local estrogen administration. Methods Venous occlusion plethysmography was used to measure forearm blood flow (FBF) in 8 older (age = 59 ± 1 years) healthy, non‐obese (BMI = 23 ± 1 kg/m 2 ) women. FBF was measured at baseline and during an intra‐arterial infusion of acetylecholine (ACH) at 1.0, 2.0, 4.0, and 8.0 μg/100 ml tissue/min, sodium nitroprusside (NTP) at 0.25, 0.5, 1.0 and 2.0 ug/100 ml tissue/min and terbutaline (β 2 agonist) at 0.1, 0.5, 1.0, 2.0 μg/100 ml tissue/min before (with dextrose co‐infusion) and during acute, local intra‐arterial infusion of estrogen (20 ηg/mL at 1 mL/min). Forearm vascular conductance (FVC) was calculated as FBF divided by mean arterial pressure. Area under the curve (AUC) was calculated for the absolute FVC and percent baseline FVC of ACH, NTP and terbutaline. Results There were no significant differences in FVC with estrogen infusion as compared to control during ACH, NTP and all terbutaline doses except dose 2 of ACH (Table 1). The AUC are not significantly different during estrogen (p>0.05) as compared to control for ACH, NTP and terbutaline (figure 1). Conclusions These data suggest that acute administration of estrogen, which corresponds to the endogenous levels of estrogen seen in premenopausal women during mid‐cycle, does not augment the β 2 ‐adrenergic vasodilator responses in postmenopausal women. Additionally, these data suggest that estrogen infusion does not increase the endothelial dependent and independent vasodilatory capacity in postmenopausal women. Support or Funding Information HL83947 (MJJ) and Mayo Clinic Women's Health Scholarship (K12 HD065987). This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .

Acute systemic induced inflammation negatively affects arterial function in young healthy adults. An acute bout of aerobic exercise reduces arterial stiffness and improves endothelial function. Therefore, we evaluated endothelial function and wave reflection in older adults in response to acute systemic inflammation and the effect of moderate intensity endurance exercise immediately prior to induced inflammation. 59 healthy volunteers (range 55 – 75 years) were randomly allocated to an exercise or control group. Arterial function and inflammatory markers were measured at baseline, 24 h and 48 h after influenza vaccine and sham injections. CRP increased approximately 1.5 times, 24 and 48 h after vaccination while IL‐6 increased 24 hours after vaccination compared to the sham injection. Unexpectedly, arterial function was unaltered (Table). Inflammation and endothelial function were dissociated following vaccine‐induced acute systemic inflammation in older adults. Acute exercise prior to vaccination had no effect of inflammation or vascular function. Support: AHA #10PRE3500083 (SMR).

Introduction Heart rate variability (HRV), blood pressure variability (BPV) and baroreflex sensitivity (BRS), measures of autonomic nervous system function, are associated with cardiovascular (CV) outcome. African Americans (AA) have an increased prevalence of CV disorders in comparison to Caucasians (C). Purpose To determine race specific responses in BPV, BRS and HRV before and after maximal exercise. Methods 37 AA and 37 C (24 years) underwent maximal exercise on a cycle ergometer. BPV, BRS and HRV measurements were assessed using finger plethysmography before and after exercise. Data were log transformed and pre‐and post‐max test values were compared by race. Results Acute exercise significantly decreased BRS, LF‐HRV and HF‐HRV and significantly increased LF/HF‐HRV in both AA and C. With exercise, C significantly decreased measures of BRS and HRV more compared to AA; BRS‐SAPRRI transfer mean (C: 2.65±.54 to 1.09±.81 versus AA: 2.70±.40 to 1.70±.92), BRS‐down down (C: 3.21±.55 to 1.74±.49 versus AA: 3.28±1.0 to 2.2±.71), HRV‐LF (C: 6.39±.86 to 3.68±1.42 versus AA: 6.37±1.24 to 5.18±2.14) and HRV‐HF (C: 7.38±1.23 to 3.53±1.73 versus AA: 7.51±1.09 to 5.38±2.16). Conclusion C exhibited increased vagal withdrawal and greater reductions in BRS compared to AA in response to acute exercise. The impact of these racial differences in autonomic control on CV risk needs further investigation.

We tested the hypothesis that reduced nitric oxide (NO) bioavailability contributes to the attenuated peak and total vasodilation following single muscle contractions in older adults. Young (n=8; 25 ± 2 yr) and older (n=9; 67 ± 2 yr) adults performed single forearm contractions at 10, 20 and 40% of maximum during saline infusion (control) and NO synthase (NOS) inhibition via L‐NMMA. Brachial artery diameter and velocities were measured using Doppler ultrasound and forearm vascular conductance (FVC) was calculated from blood flow (ml/min) and blood pressure (mmHg). Peak and total vasodilator responses (ΔFVC from baseline) were attenuated in older adults at all intensities (P < 0.05). NOS inhibition reduced the peak ΔFVC at 10% (95 ± 13 vs. 59 ± 10), 20% (134 ± 11 vs. 90 ± 12) and 40% (222 ± 30 vs. 143 ± 24) in young subjects (P < 0.05 for all) and in older adults at 10% (61 ± 5 vs. 48 ± 7, P < 0.05) and 20% (90 ± 8 vs. 70 ± 8, P < 0.05), but not 40% (129 ± 13 vs. 105 ± 11, P = 0.12). The relative (%) reduction in peak ΔFVC due to NOS inhibition was greater in young vs. older adults at 20% (−36 ± 5 vs. −22 ± 5%, P < 0.05) and 40% (−35 ± 7 vs. −17 ± 7%, P < 0.05). The reduction in the total vasodilator response (area under the curve) with NOS inhibition was also greater in young vs. older adults at 20 and 40%. Our data suggest that contraction‐induced rapid vasodilation is mediated in part by NO; however, it appears the NO contribution in the response is greater in young adults.

Hyperoxia can cause substantial reductions in peripheral and coronary blood flow at rest and during exercise. We tested the hypothesis that hyperoxia may increase the time for forearm blood flow (FBF) to reach steady state (SS) levels during exercise. Young (n=11; 28±2yr) healthy adults performed rhythmic forearm contractions at 10% of their maximum voluntary contraction for 5 minutes. Each duty cycle consisted of 1 second contraction and 2 second relaxation. Brachial artery diameters and velocities were measured using Doppler Ultrasound and forearm blood flow (ml/min) was calculated from the mean velocity and diameter. The dynamics of FBF at the onset of exercise were assessed by calculating the slope of the FBF response for every duty cycle between baseline and steady state, and the number of duty cycles to reach steady state. The slope of the line plotted from baseline FBF to SS, had a significantly attenuated slope under hyperoxia (5.4±1.1 ml/min/cycle) as compared to normoxia (10.6±2.6 ml/min/cycle). In addition, the number of duty cycles performed under hyperoxia (33±4 cycles) was significantly higher as compared to normoxia (25±4 cycles) (P<0.02). Our data suggest that hyperoxia attenuates the contraction‐induced FBF from baseline to SS as compared to normoxia.