scholarly journals Editorial to accompany exchange of views: Role of exercise pressor reflex in control of ventilation during exercise

2020 ◽  
Vol 105 (12) ◽  
pp. 2258-2259
Author(s):  
Paul J. Fadel
Keyword(s):  
Control Of Ventilation ◽  
Exercise Pressor Reflex ◽  
Pressor Reflex

The role of acid sensing ion channels in the exercise pressor reflex

2007 ◽  
Vol 21 (5) ◽  
Author(s):  
Shawn G. Hayes ◽  
Angela E. Kindig ◽  
Marc P. Kaufman
Keyword(s):  
Ion Channels ◽  
Exercise Pressor Reflex ◽  
Acid Sensing Ion Channels ◽  
Pressor Reflex

scholarly journals The role of the cyclooxygenase products in evoking sympathetic activation in exercise

2007 ◽  
Vol 293 (3) ◽  
pp. H1861-H1868 ◽  
Author(s):  
Jian Cui ◽  
Patrick McQuillan ◽  
Afsana Momen ◽  
Cheryl Blaha ◽  
Raman Moradkhan ◽  
...  
Keyword(s):  
Animal Studies ◽  
Muscle Sympathetic Nerve Activity ◽  
Prostaglandin Synthesis ◽  
Pharmacological Agents ◽  
Exercise Pressor Reflex ◽  
Exercise Blood Pressure ◽  
Before And After ◽  
Pressor Reflex ◽  
Bier Block

Animal studies suggest that prostaglandins in skeletal muscles stimulate afferents and contribute to the exercise pressor reflex. However, human data regarding a role for prostaglandins in this reflex are varied, in part because of systemic effects of pharmacological agents used to block prostaglandin synthesis. We hypothesized that local blockade of prostaglandin synthesis in exercising muscles could attenuate muscle sympathetic nerve activity (MSNA) responses to fatiguing exercise. Blood pressure (Finapres), heart rate, and MSNA (microneurography) were assessed in 12 young healthy subjects during static handgrip and postexercise muscle ischemia (PEMI) before and after local infusion of 6 mg of ketorolac tromethamine in saline via Bier block (regional intravenous anesthesia). In the second experiment ( n = 10), the same amount of saline was infused via the Bier block. Ketorolac Bier block decreased the prostaglandins synthesis to ∼33% of the baseline. After ketorolac Bier block, the increases in MSNA from the baseline during the fatiguing handgrip was significantly lower than that before the Bier block (before ketorolac: Δ502 ± 111; post ketorolac: Δ348 ± 62%, P = 0.016). Moreover, the increase in total MSNA during PEMI after ketorolac was significantly lower than that before the Bier block ( P = 0.014). Saline Bier block had no similar effect. The observations indicate that blockade of prostaglandin synthesis attenuates MSNA responses seen during fatiguing handgrip and suggest that prostaglandins contribute to the exercise pressor reflex.

scholarly journals NADPH oxidase-derived reactive oxygen species in skeletal muscle modulates the exercise pressor reflex

2009 ◽  
Vol 107 (2) ◽  
pp. 450-459 ◽  
Author(s):  
Han-Jun Wang ◽  
Yan-Xia Pan ◽  
Wei-Zhong Wang ◽  
Irving H. Zucker ◽  
Wei Wang
Keyword(s):  
Blood Pressure ◽  
Reactive Oxygen Species ◽  
Nadph Oxidase ◽  
Pressor Response ◽  
Oxidase Inhibitor ◽  
Oxygen Species ◽  
Exercise Pressor Reflex ◽  
Pressor Reflex ◽  
Stimulation Of

Muscle metabolic by-products during exercise, such as K+, lactic acid, ATP, H+, and phosphate, are well established to be involved in the reflex cardiovascular response to static muscle contraction. However, the role of muscle reactive oxygen species (ROS), a metabolic by-product during muscle contraction, in the exercise pressor reflex (EPR) has not been investigated in detail. In the present study, we evaluated the role of muscle ROS in the EPR in a decerebrate rat model. We hypothesized that muscle NADPH oxidase-derived ROS contributes to sensitization of the EPR. Thus the rise in blood pressure and heart rate in response to a 30-s static contraction induced by electrical stimulation of L4/L5 ventral roots was compared before and after hindlimb arterial infusion of the redox agents: diethyldithiocarbamate, a superoxide dismutase inhibitor; the superoxide dismutase mimetic 4-hydroxy-2,2,6,6-tetramethyl piperidine 1-oxyl (tempol); the free radical scavenger dimethylthiourea; a NADPH oxidase inhibitor, apocynin; and a xanthine oxidase inhibitor, allopurinol. The EPR-induced pressor response was augmented after treatment with diethyldithiocarbamate and was attenuated after treatment with tempol, dimethylthiourea, and apocynin. Treatment with allopurinol did not affect the EPR function. None of the drug's affected the EPR heart rate response. In addition, neither the pressor response to electrical stimulation of the central end of dorsal roots, nor femoral blood flow was affected by any treatment. These data suggest that NADPH oxidase-derived muscle ROS plays an excitatory role in the EPR control of blood pressure.

scholarly journals The Role of ASIC Channels in the Exercise Pressor Reflex

2006 ◽  
Vol 38 (Suppl 1) ◽  
pp. S16
Author(s):  
Shawn G. Hayes ◽  
Angela E. Kindig ◽  
Jong Kyung Kim ◽  
Marc P. Kaufman
Keyword(s):  
Exercise Pressor Reflex ◽  
Pressor Reflex

scholarly journals Role of the PAG in the Exercise Pressor Reflex during Varying Intensity of Activity

2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Shanika Deshani Basnayake ◽  
Alexander L Green ◽  
Tipu Z Aziz ◽  
David J Paterson
Keyword(s):  
Exercise Pressor Reflex ◽  
Pressor Reflex
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