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

Jian Cui, Patrick McQuillan, Afsana Momen, Cheryl Blaha, Raman Moradkhan, Vernon Mascarenhas, Cynthia Hogeman, Anandi Krishnan, Lawrence Sinoway

Research output: Contribution to journalArticle

20 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume293
Issue number3
DOIs
StatePublished - Sep 1 2007

Fingerprint

Prostaglandin-Endoperoxide Synthases
Ketorolac
Prostaglandins
Exercise
Muscles
Reflex
Ischemia
Ketorolac Tromethamine
Intravenous Anesthesia
Conduction Anesthesia
Myocardium
Healthy Volunteers
Skeletal Muscle
Heart Rate
Pharmacology
Blood Pressure

All Science Journal Classification (ASJC) codes

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

Cui, Jian ; McQuillan, Patrick ; Momen, Afsana ; Blaha, Cheryl ; Moradkhan, Raman ; Mascarenhas, Vernon ; Hogeman, Cynthia ; Krishnan, Anandi ; Sinoway, Lawrence. / The role of the cyclooxygenase products in evoking sympathetic activation in exercise. In: American Journal of Physiology - Heart and Circulatory Physiology. 2007 ; Vol. 293, No. 3.
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The role of the cyclooxygenase products in evoking sympathetic activation in exercise. / Cui, Jian; McQuillan, Patrick; Momen, Afsana; Blaha, Cheryl; Moradkhan, Raman; Mascarenhas, Vernon; Hogeman, Cynthia; Krishnan, Anandi; Sinoway, Lawrence.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 293, No. 3, 01.09.2007.

Research output: Contribution to journalArticle

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AU - McQuillan, Patrick

AU - Momen, Afsana

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AB - 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.

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