Search

This study was undertaken to evaluate the effect of treatment with prednisone or verapamil on plasma met-enkephalin (ME), neutrophil met-enkephalin containing peptides (NMECP) and free and conjugated plasma catecholamines (CA) in cluster headache (CH) patients. After obtaining a basal sample, patients were randomly selected to be treated with either verapamil (n = 5) or prednisone (n = 5). A second blood sample was obtained 10 days after starting treatment. At this time all patients were free of symptoms. ME (0.49 +/- 0.10 pmol/mL) and NMECP (35.1 +/- 2.4 pmol/mg protein) levels after prednisone treatment were significantly higher (P < 0.05) than in basal conditions (0.29 +/- 0.08 pmol/mL and 27.14 +/- 2.4 pmol/mg protein), while no differences were found in catecholamine levels. No differences in ME, NMECP or CA were found during verapamil treatment. Our results suggest that in CH the two drugs act through different mechanisms. The relief of the bout obtained with prednisone may be related to the opioid system stimulation observed in these patients.

We have previously demonstrated an increase in plasma met-enkephalin levels during the pain attacks in episodic cluster headache. The present study was undertaken in order to clarify the source of the plasma met-enkephalin increase. Recent evidence has shown that peripheral blood polymorphonuclear cells contain peptides derived from the proenkephalin A system, which can be released by specific stimuli. We studied neutrophil met-enkephalin containing peptides (NMECP) in 27 episodic cluster headache patients: 24 in a cluster period (6 of them during a pain attack), and 3 in the remission period. Neutrophil met-enkephalin containing peptide levels (after sequential enzymatic digestion with trypsin and carboxypeptidase B) were determined by radioimmunoassay with specific antiserum. Neutrophil peptide concentration (pmol/mg prot) was lower (p less than 0.01) in patients during the pain attack (14.4 +/- 0.36) than after their pain had subsided (36.7 +/- 0.31) and lower than in the remission period patients (35.8 +/- 0.4). We conclude that neutrophil met-enkephalin containing peptides decrease during pain in episodic cluster headache, and that they may be involved in the concomitant plasma met-enkephalin increase.

We measured methionine-enkephalin (MET) in platelets and platelet-poor-plasma of drug-free patients with classic migraine, common migraine or tension headache (TH). Migraineurs were studied both between and during attacks. TH patients were characterized by low platelet-MET and high plasma-MET levels, whereas migraine patients showed high platelet-MET and reduced plasma-MET levels. During migraine attacks both platelet and plasma-MET concentrations increased considerably. We suggest that determination of MET levels in platelets and plasma may be a useful marker to discriminate between TH and common migraine. The rise in MET during attacks may be directed against the ictal increase of serotonin.

The effects of either hypotension induced by sodium nitroprusside or hexamethonium or hypertension produced by angiotensin II or noradrenaline on the circulating levels of methionine enkephalin ([Met]enkephalin)-like immunoreactivity (MLI), adrenaline and noradrenaline in anaesthetized greyhounds were examined. Nitroprusside infusions (200 and 400 micrograms min-1) induced a fall in blood pressure accompanied by significant rises in plasma MLI and catecholamine concentrations. Concomitant administration of a high dose of naloxone did not alter the fall in blood pressure produced by nitroprusside but was associated with greater rises in circulating MLI and catecholamines when compared to nitroprusside alone, suggesting that [Met]enkephalin is not involved in the hypotensive action of nitroprusside. Intravenous hexamethonium (2.5 mg kg-1) provoked a fall in blood pressure which was not associated with any changes in plasma MLI. However, it produced a fall in plasma noradrenaline and a rise in plasma adrenaline. Thus it appears that neural mechanisms are required, at least in part, for the release of MLI. Angiotensin II (1.25 micrograms kg-1 min-1) and noradrenaline (8 micrograms kg-1 min-1) infusions produced an elevation in blood pressure without altering the circulating MLI levels. Study of the molecular forms of circulating MLI, before and during hypotension, revealed that the large molecular weight enkephalin-containing peptides with approximate molecular sizes of 18kD and 8kD were the predominant forms both in the basal and stimulated states. It is concluded that circulating [Met]enkephalin is not involved in the tonic control of blood pressure but it may modulate catecholamine release following hypotension as part of the stress response.