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Cyclooxygenase Inhibition Attenuates the Muscle Sympathetic Nerve Activity Responses to Venous Distension in Humans
Author(s) -
Cui Jian,
McQuillan Patrick,
Blaha Cheryl,
Sinoway Lawrence
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.649.5
Subject(s) - medicine , distension , anesthesia , saline , reflex , microneurography , blockade , blood pressure , heart rate , baroreflex , receptor
We have shown that venous distension induced by saline infusion into veins of an arterially occluded arm evokes reflex increases in muscle sympathetic nerve activity (MSNA) and blood pressure (BP) in humans. Recently, Yamauchi and colleagues examined this venous distension reflex in rats and showed that cyclooxygenase blockade with indomethacin attenuated the reflex pressor response. We hypothesized that blockade of prostaglandin synthesis could attenuate MSNA responses to venous distension in humans. BP (Finapres), heart rate, and MSNA (microneurography) were assessed in 11 young healthy subjects during infusion of 6 mg ketorolac tromethamine in 40 ml saline into veins of an arterially occluded arm. In the second experiment, the same amount of saline was infused (control trial). MSNA significantly rose towards to the end of infusion of saline (18.1±2.1 to 27.0±2.7 bursts/min, P<0.01), while no significant change was observed in the ketorolac trial (19.0±2.2 to 22.7±3.2 bursts/min, P=0.77). BP significantly rose towards to the end of infusion in the both trials, and the BP response in ketorolac trial tended to be less than that in saline trial (P=0.07). These observations indicate that blockade of prostaglandin synthesis may attenuate MSNA and BP responses to distension of veins, and suggest that prostaglandins may contribute to the venous distension reflex.