Effects of intravenous magnesium infusion on in vivo release of acetylcholine and catecholamine in rat adrenal medulla

• Published in: Autonomic neuroscience Vol. 177; no. 2; pp. 123 - 128
• Main Authors: Komaki, Fumiaki, Akiyama, Tsuyoshi, Yamazaki, Toji, Kitagawa, Hirotoshi, Nosaka, Syuichi, Shirai, Mikiyasu
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 01.10.2013
• Subjects: Acetylcholine; Acetylcholine - metabolism; Acetylcholine - secretion; Adrenal Medulla - drug effects; Adrenal Medulla - secretion; Advanced Basic Science; Anesthetized rats; Animals; Catecholamines - metabolism; Catecholamines - secretion; Epinephrine; Infusions, Intravenous; Magnesium; Magnesium Sulfate - administration & dosage; Male; Medical Education; Microdialysis - methods; Microdialysis technique; Norepinephrine; Rats; Rats, Wistar; Anesthetized rats; Epinephrine; Acetylcholine; Norepinephrine; Magnesium; Microdialysis technique
• ISSN: 1566-0702; 1872-7484
• DOI: 10.1016/j.autneu.2013.03.004

Abstract We applied microdialysis technique to the left adrenal medulla of anesthetized rats and examined the effects of intravenous Mg 2 + infusion on presynaptic acetylcholine (ACh) release and postsynaptic catecholamine release induced by electrical stimulation of splanchnic nerves. The dialysis probes were perfused with Ringer's solution containing neostigmine. Low-dose MgSO4 (25 μmol/kg/min for 30 min i.v.) increased mean plasma Mg 2 + concentration to 2.5 mM; the administration suppressed norepinephrine (NE) release by approximately 30% and epinephrine (Epi) release by approximately 20%, but did not affect ACh release. High-dose MgSO4 (50 μmol/kg/min for 30 min i.v.) increased mean plasma Mg 2 + concentration to 3.8 mM; the administration suppressed ACh release by approximately 25%, NE release by approximately 60% and Epi release by approximately 45%. Administration of Na2 SO4 (50 μmol/kg/min for 30 min i.v.) did not change the release of ACh, NE or Epi. Local administration of nifedipine (200 μM) suppressed NE release by approximately 40% and Epi release by approximately 30%, but did not affect ACh release. In the presence of nifedipine, low-dose MgSO4 did not suppress the release of ACh, or further suppress NE or Epi compared to nifedipine alone, but high-dose MgSO4 suppressed ACh release by approximately 25% and further suppressed NE release by approximately 60% and Epi release by approximately 50% compared to nifedipine alone. In conclusion, intravenous administration of Mg 2 + inhibits both presynaptic ACh release and postsynaptic catecholamine release in the adrenal medulla, but L-type Ca 2 + channel-controlled catecholamine release may be more sensitive to Mg 2 + than non-L-type Ca 2 + channel-controlled ACh release.