Nitric oxide in the potassium-induced response of the rat middle cerebral artery: a possible permissive role

Nitric oxide in the potassium-induced response of the rat middle cerebral artery: a possible... In the middle cerebral artery (MCA), the presence of nitric oxide (NO) is responsible for maintaining a more dilated state than in its absence during increases in extracellular K + and osmolality. The purpose of the present study was to determine whether the involvement of NO was due to (a) a direct effect of the K + /osmolality ( K hyper ) on the endothelium or (b) a ‘permissive’ role of NO. MCAs (approximately 210 μm o.d.) were isolated, cannulated with glass micropipettes, and pressurized to 85 mmHg. When K + (KCl) in the extraluminal bath was increased to 21 mM, the diameter increased by 15–20% with the magnitude of dilation diminishing with further increases in K hyper . The addition of N G -nitro- l -arginine methyl ester ( l -NAME, 10 −5 mM), an inhibitor of nitric oxide synthase, had no significant effect on dilations at lower K hyper concentrations but constricted the arteries relative to the control at 51, 66, and 81 mM K hyper . In the presence of l -NAME, the addition of an exogenous NO donor, S -nitroso- N -acetylpenicillamine (SNAP, 10 −8 M) or an analog of cGMP, 8-bromo-cGMP (6×10 −5 M), tended to restore the response of K hyper to near the original response. We conclude that the basal release of NO from the endothelium plays a permissive role in the K hyper -induced response. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Brain Research Elsevier

Nitric oxide in the potassium-induced response of the rat middle cerebral artery: a possible permissive role

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Publisher
Elsevier
Copyright
Copyright © 2001 Elsevier Science B.V.
ISSN
0006-8993
D.O.I.
10.1016/S0006-8993(00)03121-8
Publisher site
See Article on Publisher Site

Abstract

In the middle cerebral artery (MCA), the presence of nitric oxide (NO) is responsible for maintaining a more dilated state than in its absence during increases in extracellular K + and osmolality. The purpose of the present study was to determine whether the involvement of NO was due to (a) a direct effect of the K + /osmolality ( K hyper ) on the endothelium or (b) a ‘permissive’ role of NO. MCAs (approximately 210 μm o.d.) were isolated, cannulated with glass micropipettes, and pressurized to 85 mmHg. When K + (KCl) in the extraluminal bath was increased to 21 mM, the diameter increased by 15–20% with the magnitude of dilation diminishing with further increases in K hyper . The addition of N G -nitro- l -arginine methyl ester ( l -NAME, 10 −5 mM), an inhibitor of nitric oxide synthase, had no significant effect on dilations at lower K hyper concentrations but constricted the arteries relative to the control at 51, 66, and 81 mM K hyper . In the presence of l -NAME, the addition of an exogenous NO donor, S -nitroso- N -acetylpenicillamine (SNAP, 10 −8 M) or an analog of cGMP, 8-bromo-cGMP (6×10 −5 M), tended to restore the response of K hyper to near the original response. We conclude that the basal release of NO from the endothelium plays a permissive role in the K hyper -induced response.

Journal

Brain ResearchElsevier

Published: Jan 19, 2001

References

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