The effects of prostaglandin inhibition on the sympathetic and pressor responses to muscular contraction and postcontraction muscle ischemia

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1992-06-05
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Virginia Tech
Abstract

The purpose of this study was to determine the effect of prostaglandin (PG) inhibition on the sympathetic and pressor responses to isometric handgrip (HG) at 40% of maximal voluntary contraction (MVC) to exhaustion and postcontraction muscle ischemia (PC). To accomplish this heart rate (HR), arterial pressure (n=10) and plasma norepinephrine (NE) levels (n=8) were measured in 10 healthy male subjects during HG at 40% of MVC to exhaustion and during PC. The subjects were given a double-blind administration of either placebo (PLAC) or a single 100 mg dose of indomethacin (IND). The order of administration was counterbalanced and a one week drug washout period was provided between conditions. Mean arterial pressure increased 25±5 vs. 22±4 mmHg during the second minute of HG and 26±2 vs. 21±5 during the last minute of PC in PLAC vs. IND (P>.05), respectively. Heart rate was increased 21±4 vs. 17±3 bpm during the second minute of HG in PLAC vs. IND (P>.05), respectively and returned to control values during PC in both trials. Plasma NE increased 343189 vs. 289±89 pg/ml after HG and 67514132 vs. 6324132 pg/ml after PC (P>.05) in PLAC vs. IND, respectively. Therefore, PG inhibition does not alter sympathetic or arterial pressure responses during sustained isometric exercise in humans. This may suggest that 1) PGs not important in metaboreceptor stimulation of sympathetic or pressor responses to sustained isometric contractions in humans or 2) PGs may play only a small role in the regulation of these variables which may be masked by the effects of other stimuli.

Index terms: prostaglandins, pressor reflex, muscle sympathetic nerve activity, static exercise

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