Glutamate neurotransmission and nitric oxide interaction within the ventrolateral medulla during cardiovascular responses to muscle contraction.
We previously reported that nitric oxide, within the RVLM and CVLM, plays an opposing role in modulating cardiovascular responses during static muscle contraction [B.J. Freda, R.S. Gaitonde, R. Lillaney, A. Ally, Cardiovascular responses to muscle contraction following microdialysis of nitric oxide precursor into ventrolateral medulla, Brain Res. 828 (1999) 60-67]. In this study, we determined whether the effects of administering L-arginine, a precursor for the synthesis of nitric oxide, and N(G)-monomethyl-L-arginine (L-NMMA), a nitric oxide synthase inhibitor, into the rostral (RVLM) and caudal (CVLM) ventrolateral medulla on cardiovascular responses elicited during static muscle contraction were mediated via an alteration of localized glutamate concentrations using microdialysis techniques. In experiments within the RVLM (n=8), muscle contraction increased MAP and HR by 21+/-2 mmHg and 22+/-3 bpm, respectively. Glutamate increased from 1.1+/-0.4 to 4.4+/- 0.6 ng/5 microl measured from bilateral RVLM areas. Microdialysis of L-arginine (1.0 microM) for 30 min attenuated the contraction-evoked increases in MAP, HR, and glutamate levels. After subsequent microdialysis of L-NMMA (1.0 microM) into the RVLM, contraction augmented the pressor and tachycardic responses and glutamate release. In experiments within CVLM (n=8), muscle contraction increased MAP and HR by 22+/-3 mmHg and 20+/-2 bpm, respectively. Glutamate increased from 0.8+/-0. 4 to 3.6+/-0.6 ng/5 microl measured from the CVLM. L-Arginine augmented the cardiovascular responses and glutamate release and L-NMMA attenuated all the effects. Results suggest that nitric oxide within the RVLM and CVLM plays opposing roles in modulating cardiovascular responses during static exercise via decreasing and increasing, respectively, extracellular glutamate levels.
Ishide
T
T
Third Department of Internal Medicine, Chiba University School of Medicine, 260, Chiba, Japan.
Hara
Y
Y
Maher
T J
TJ
Ally
A
A
D000818:Animals; D001120:Arginine / Q000008:administration & dosage / Q000494:pharmacology; D017704:Baroreflex / Q000502:physiology; D001794:Blood Pressure / Q000187:drug effects; D002320:Cardiovascular Physiological Phenomena; D005110:Extracellular Space / Q000378:metabolism; D005260:Female; D018698:Glutamic Acid / Q000502:physiology*; D006339:Heart Rate / Q000187:drug effects; D008526:Medulla Oblongata / Q000187:drug effects / Q000502:physiology*; D017551:Microdialysis; D009043:Motor Activity / Q000502:physiology; D009119:Muscle Contraction / Q000187:drug effects / Q000502:physiology*; D009569:Nitric Oxide / Q000502:physiology*; D009994:Osmolar Concentration; D051381:Rats; D017207:Rats, Sprague-Dawley; D009435:Synaptic Transmission / Q000502:physiology*
D009569:Nitric Oxide; D018698:Glutamic Acid; D001120:Arginine