title: Changes in extracellular glutamate and pressor response during muscle contraction following AMPA-receptor blockade in the RVLM and CVLM.
abstract: We examined whether modulation of cardiovascular responses by administering 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, an AMPA-receptor antagonist) into the rostral (RVLM) or caudal (CVLM) ventrolateral medulla are mediated via changes in extracellular levels of glutamate. Microdialysis probes were inserted bilaterally into the RVLM or the CVLM. For the RVLM experiments (n=8), muscle contraction for 2 min increased mean arterial pressure (MAP) and heart rate (HR) by 18+/-3 mmHg and 24+/-5 bpm, respectively. Extracellular glutamate concentrations increased from 1.5+/-0.3 to 4.3+/-0.9 ng/5 microl during the contraction. Microdialysis of CNQX (1.0 microM) for 30 min into the RVLM attenuated the increases in MAP, HR, and glutamate concentration in response to a muscle contraction (8+/-2 mmHg, 11+/-3 bpm, and 2.2+/-0.7 ng/5 microl, respectively). Developed tensions did not change during contractions before and after CNQX. Microdialysis of CNQX into the CVLM (n=8) potentiated the contraction-evoked responses in MAP (19+/-3 vs. 34+/-3 mmHg) and HR (25+/-4 vs. 49+/-5 bpm) without a change in developed tension. Following CNQX perfusion into the CVLM, the levels of extracellular glutamate in the CVLM were also augmented during the contraction. Results suggests that AMPA-receptors within the RVLM and CVLM differentially modulate cardiovascular responses during static muscle contraction via increasing and decreasing, respectively, extracellular glutamate concentrations.
authors.affiliation: Department of Physiology, College of Osteopathic Medicine, University of New England, Biddeford, ME 04055, USA.
authors.forename: R
authors.initials: R
authors.lastname: Lillaney
authors.forename: T J
authors.initials: TJ
authors.lastname: Maher
authors.forename: P
authors.initials: P
authors.lastname: Chaiyakul
authors.forename: A
authors.initials: A
authors.lastname: Ally
mesh_terms: D018750:6-Cyano-7-nitroquinoxaline-2,3-dione / Q000494:pharmacology; D000818:Animals; D001794:Blood Pressure; D004558:Electric Stimulation; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D005110:Extracellular Space / Q000378:metabolism; D005260:Female; D018698:Glutamic Acid / Q000378:metabolism*; D006339:Heart Rate; D008526:Medulla Oblongata / Q000737:chemistry / Q000187:drug effects / Q000502:physiology*; D017551:Microdialysis; D009119:Muscle Contraction / Q000502:physiology*; D009129:Muscle Tonus / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D018091:Receptors, AMPA / Q000037:antagonists & inhibitors*; D012018:Reflex / Q000502:physiology; D013979:Tibial Nerve / Q000502:physiology; D014661:Vasoconstriction / Q000502:physiology
chemical_list: D018691:Excitatory Amino Acid Antagonists; D018091:Receptors, AMPA; D018698:Glutamic Acid; D018750:6-Cyano-7-nitroquinoxaline-2,3-dione