scholarly journals Effect of cyclooxygenase inhibition on the inspiratory muscle metaboreflex-induced cardiovascular consequences in men

2017 ◽  
Vol 123 (1) ◽  
pp. 197-204 ◽  
Author(s):  
Joshua R. Smith ◽  
Kaylin D. Didier ◽  
Shane M. Hammer ◽  
Andrew M. Alexander ◽  
Stephanie P. Kurti ◽  
...  

Inspiratory muscle metaboreflex activation increases mean arterial pressure (MAP) and limb vascular resistance (LVR) and decreases limb blood flow (Q̇L). Cyclooxygenase (COX) inhibition has been found to attenuate limb skeletal muscle metaboreflex-induced increases in muscle sympathetic nerve activity. We hypothesized that compared with placebo (PLA), COX inhibition would attenuate inspiratory muscle metaboreflex-induced 1) increases in MAP and LVR and 2) decreases in Q̇L. Seven men (22 ± 1 yr) were recruited and orally consumed ibuprofen (IB; 10 mg/kg) or PLA 90 min before performing the cold pressor test (CPT) for 2 min and inspiratory resistive breathing task (IRBT) for 14.9 ± 2.0 min at 65% of maximal inspiratory pressure. Breathing frequency was 20 breaths/min with a 50% duty cycle during the IRBTs. MAP was measured via automated oscillometry, Q̇L was determined via Doppler ultrasound, and LVR was calculated as MAP divided by Q̇L. Electromyography was recorded on the leg to ensure no muscle contraction occurred. The 65% IRBT led to greater increases ( P = 0.02) in 6-keto-prostaglandin-F1α with PLA compared with IB. IB, compared with PLA, led to greater ( P < 0.01) increases in MAP (IB: 17 ± 7 mmHg vs. PLA: 8 ± 5 mmHg) and LVR (IB: 69 ± 28% vs. PLA: 52 ± 22%) at the final minute of the 65% IRBT. The decrease in Q̇L was not different ( P = 0.72) between IB (−28 ± 11%) and PLA (−27 ± 9%) at the final minute. The increase in MAP during the CPT was not different ( P = 0.87) between IB (25 ± 11 mmHg) and PLA (24 ± 6 mmHg). Contrary to our hypotheses, COX inhibition led to greater inspiratory muscle metaboreflex-induced increases in MAP and LVR. NEW & NOTEWORTHY Cyclooxygenase (COX) products play a role in activating the muscle metaboreflex. It is not known whether COX products contribute to the inspiratory muscle metaboreflex. Herein, we demonstrate that COX inhibition led to greater increases in blood pressure and limb vascular resistance compared with placebo during inspiratory muscle metaboreflex activation.

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

2020 ◽  
Vol 319 (3) ◽  
pp. R288-R295
Author(s):  
M. L. Keller-Ross ◽  
H. A. Cunningham ◽  
J. R. Carter

Prior longitudinal work suggests that blood pressure (BP) reactivity to the cold pressor test (CPT) helps predict hypertension; yet the impact of age and sex on hemodynamic and neural responsiveness to CPT remains equivocal. Forty-three young (21 ± 1yr, means ± SE) men (YM, n = 20) and women (YW, n = 23) and 16 older (60 ± 1yr) men (OM, n = 9) and women (OW, n = 7) participated in an experimental visit where continuous BP (finger plethysmography) and muscle sympathetic nerve activity (MSNA; microneurography) were recorded during a 3- to 5-min baseline and 2-min CPT. Baseline mean arterial pressure (MAP) was greater in OM than in YM (92 ± 4 vs. 77 ± 1 mmHg, P < 0.01), but similar in women ( P = 0.12). Baseline MSNA incidence was greater in OM [69 ± 6 bursts/100 heartbeats (hb)] than in OW (44 ± 7 bursts/100 hb, P = 0.02) and lower in young adults (YM: 17 ± 3 vs. YW: 16 ± 2 bursts/100 hb, P < 0.01), but similar across the sexes ( P = 0.83). However, when exposed to the CPT, MSNA increased more rapidly in OW (Δ43 ± 6 bursts/100 hb; group × time, P = 0.01) compared with OM (Δ15 ± 3 bursts/100 hb) but was not different between YW (Δ30 ± 3 bursts/100 hb) and YM (Δ33 ± 4 bursts/100 hb, P = 1.0). There were no differences in MAP with CPT between groups (group × time, P = 0.33). These findings suggest that OW demonstrate a more rapid initial rise in MSNA responsiveness to a CPT compared with OM. This greater sympathetic reactivity in OW may be a contributing mechanism to the increased hypertension risk in postmenopausal women.


1991 ◽  
Vol 260 (3) ◽  
pp. E379-E388 ◽  
Author(s):  
P. A. Farrell ◽  
T. J. Ebert ◽  
J. P. Kampine

The influence of an endogenous opioid peptide (EOP) antagonist (naloxone, 1.2 mg iv bolus) on muscle sympathetic nerve activity (MSNA, microneurography) was studied on 19 young male and female volunteers. Isometric handgrip, cold pressor test, and acute baroreceptor unloading with sodium nitroprusside (autonomic stresses) were carried out under two conditions, one group (n = 11) before (control responses) and after naloxone and another group (n = 8) before and after placebo saline. Monitored cardiovascular variables included heart rate, central venous pressure (jugular vein catheter), arterial blood pressure (radial artery catheter), circulating catecholamines, and forearm blood flow. At rest, cardiovascular variables and MSNA were not affected by either naloxone or saline. MSNA (total activity = burst frequency x burst amplitude/100 cardiac cycles) increased during isometric handgrip to a greater extent (30 +/- 6 vs. 16 +/- 5 arbitrary units) after naloxone compared with control trials (P less than 0.05). After naloxone, arterial systolic and diastolic blood pressures were higher during handgrip exercise. These augmented arterial pressures and MSNA responses were not evident during either the cold pressor test or the sodium nitroprusside stress. These data suggest that isometric muscle contraction elicits a sympathetic neural response that may be modified by EOP. This interaction is not evident during two other stresses, when sympathetic responses are equal to or greater than those provoked by isometric handgrip exercise.


2016 ◽  
Vol 310 (2) ◽  
pp. H300-H309 ◽  
Author(s):  
Seth W. Holwerda ◽  
Robert M. Restaino ◽  
Camila Manrique ◽  
Guido Lastra ◽  
James P. Fisher ◽  
...  

Previous studies have reported exaggerated increases in arterial blood pressure during exercise in type 2 diabetes (T2D) patients. However, little is known regarding the underlying neural mechanism(s) involved. We hypothesized that T2D patients would exhibit an augmented muscle metaboreflex activation and this contributes to greater pressor and sympathetic responses during exercise. Mean arterial pressure (MAP), heart rate (HR), and muscle sympathetic nerve activity (MSNA) were measured in 16 patients with T2D (8 normotensive and 8 hypertensive) and 10 healthy controls. Graded isolation of the muscle metaboreflex was achieved by postexercise ischemia (PEI) following static handgrip performed at 30% and 40% maximal voluntary contraction (MVC). A cold pressor test (CPT) was also performed as a generalized sympathoexcitatory stimulus. Increases in MAP and MSNA during 30 and 40% MVC handgrip were augmented in T2D patients compared with controls ( P < 0.05), and these differences were maintained during PEI (MAP: 30% MVC PEI: T2D, Δ16 ± 2 mmHg vs. controls, Δ8 ± 1 mmHg; 40% MVC PEI: T2D, Δ26 ± 3 mmHg vs. controls, Δ16 ± 2 mmHg, both P < 0.05). MAP and MSNA responses to handgrip and PEI were not different between normotensive and hypertensive T2D patients ( P > 0.05). Interestingly, MSNA responses were also greater in T2D patients compared with controls during the CPT ( P < 0.05). Collectively, these findings indicate that muscle metaboreflex activation is augmented in T2D patients and this contributes, in part, to augmented pressor and sympathetic responses to exercise in this patient group. Greater CPT responses suggest that a heightened central sympathetic reactivity may be involved.


2020 ◽  
Vol 129 (5) ◽  
pp. 1203-1213
Author(s):  
Gabrielle A. Dillon ◽  
Zachary S. Lichter ◽  
Lacy M. Alexander ◽  
Lauro C. Vianna ◽  
Jing Wang ◽  
...  

The magnitude of the increases in blood pressure and muscle sympathetic nerve activity in response to sympathoexcitatory stimuli such as static handgrip, postexercise ischemia, and the cold pressor test are commonly used to assess neurocardiovascular responsiveness. However, limited studies have comprehensively examined the reproducibility of these responses. We demonstrate that the reproducibility of the pressor response to these perturbations was very good within an individual, whereas the reproducibility of the MSNA response was less consistent.


Author(s):  
Joseph C. Watso ◽  
Mu Huang ◽  
Luke Belval ◽  
Frank A. Cimino III ◽  
Caitlin P. Jarrard ◽  
...  

Our knowledge about how low-dose (analgesic) fentanyl affects autonomic cardiovascular regulation is primarily limited to animal experiments. Notably, it is unknown if low-dose fentanyl influences human autonomic cardiovascular responses during painful stimuli in humans. Therefore, we tested the hypothesis that low-dose fentanyl reduces perceived pain and subsequent sympathetic and cardiovascular responses in humans during an experimental noxious stimulus. Twenty-three adults (10F/13M; 27±7 y; 26±3 kg•m-2, mean ± SD) completed this randomized, crossover, placebo-controlled trial during two laboratory visits. During each visit, participants completed a cold pressor test (CPT; hand in ~0.4 °C ice bath for two minutes) before and five minutes after drug/placebo administration (75 μg fentanyl or saline). We compared pain perception (100 mm visual analog scale), muscle sympathetic nerve activity (MSNA; microneurography, 11 paired recordings), and beat-to-beat blood pressure (BP; photoplethysmography) between trials (at both pre- and post-drug/placebo time points) using paired, two-tailed t-tests. Before drug/placebo administration, perceived pain (p=0.8287), Δ MSNA burst frequency (p=0.7587), and Δ mean BP (p=0.8649) during the CPT were not different between trials. After the drug/placebo administration, fentanyl attenuated perceived pain (36 vs. 66 mm, p<0.0001), Δ MSNA burst frequency (9 vs. 17 bursts/minute, p=0.0054), and Δ mean BP (7 vs. 13 mmHg, p=0.0174) during the CPT compared to placebo. Fentanyl-induced reductions in pain perception and Δ mean BP were moderately related (r=0.40, p=0.0641). These data provide valuable information regarding how low-dose fentanyl reduces autonomic cardiovascular responses during an experimental painful stimulus.


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