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.
Low dose ketamine reduces pain perception and blood pressure, but not muscle sympathetic nerve activity, responses during a cold pressor test
