The Effect of the Nitric Oxide Synthase Inhibitor N-Nitro-L-Arginine-Methyl Ester on Neuropeptide-Induced Vasodilation and Protein Extravasation in Human Skin

2003 ◽  
Vol 40 (2) ◽  
pp. 105-114 ◽  
Author(s):  
Monika Klede ◽  
Geraldine Clough ◽  
Grischa Lischetzki ◽  
Martin Schmelz
Keyword(s):  
Nitric Oxide ◽  
Methyl Ester ◽  
Nitric Oxide Synthase ◽  
Human Skin ◽  
Nitric Oxide Synthase Inhibitor ◽  
Protein Extravasation ◽  
Synthase Inhibitor ◽  
Oxide Synthase

The Nitric Oxide Synthase Inhibitor NG-nitro-L-Arginine Methyl Ester Potentiates Insulin Secretion Stimulated by Glucose and L-Arginine Independently of its Action on ATP-Sensitive K+ Channels

1998 ◽  
Vol 18 (1) ◽  
pp. 19-28 ◽  
Author(s):  
Albert Salehi ◽  
Fariborz Parandeh ◽  
Ingmar Lundquist
Keyword(s):  
Nitric Oxide ◽  
Insulin Secretion ◽  
Methyl Ester ◽  
Nitric Oxide Synthase ◽  
Insulin Release ◽  
Glucagon Secretion ◽  
Nitric Oxide Synthase Inhibitor ◽  
Insulin And Glucagon Secretion ◽  
Synthase Inhibitor ◽  
Oxide Synthase

The nature of the action of the nitric oxide synthase (NOS) inhibitor NG-nitro-L-arginine methyl ester (L-NAME) on hormone release from isolated islets was investigated. We found that glucose-induced insulin release was potentiated by L-NAME in the absence or presence of diazoxide, a potent K+ATP channel opener, as well as in the presence of diazoxide plus a depolarizing concentration of K+. At a low, physiological glucose concentration L-NAME did not influence insulin secretion induced by K+ but inhibited glucagon secretion. L-arginine-induced insulin release was potentiated by L-NAME. This potentiation was observed also in the presence of K+ plus diazoxide. Further, glucagon release induced by L-arginine as well as by L-arginine plus K+ and diazoxide was suppressed by L-NAME. The results strongly suggest that the L-NAME-induced potentiation of insulin secretion in response to glucose or L-arginine as well as the inhibitory effects on glucagon secretion are largely mediated by L-NAME directly suppressing islet NOS activity. Hence NO apparently affects insulin and glucagon secretion independently of membrane depolarization events.

Endothelial-mediated dilations of rat middle cerebral arteries by ATP and ADP

1997 ◽  
Vol 273 (3) ◽  
pp. H1472-H1477 ◽  
Author(s):  
J. You ◽  
T. D. Johnson ◽  
W. F. Childres ◽  
R. M. Bryan
Keyword(s):  
Nitric Oxide ◽  
Methyl Ester ◽  
Nitric Oxide Synthase ◽  
Cerebral Arteries ◽  
Nitric Oxide Synthase Inhibitor ◽  
Middle Cerebral Arteries ◽  
Synthase Inhibitor ◽  
Oxide Synthase ◽  
Maximum Removal

The hypothesis that ATP and ADP produce dilations of rat middle cerebral arteries (MCAs) by different mechanisms was tested. Vessel diameters were measured from pressurized, perfused MCAs after application of different agonists. The luminal administration of ATP and ADP elicited concentration-dependent dilations (35% maximum). Removal of endothelium abolished the dilation to intraluminal ATP and attenuated the dilation to intraluminal ADP. The dilations to ATP were abolished with N omega-nitro-L-arginine methyl ester (L-NAME; 10 microM), a nitric oxide synthase inhibitor, at ATP concentrations of 1 microM and below. However, at concentrations of 10 microM ATP and above, L-NAME had no effect on the response. The dilations to ADP were attenuated by L-NAME to the same degree as removal of endothelium. The mechanism for dilation by ATP was identical to that of UTP, a selective P2u purinoceptor agonist. The mechanism of dilation by ADP was similar to that of 2-methylthioadenosine 5'-triphosphate, a selective P2y purinoceptor agonist. We conclude that ATP and ADP elicit dilations of rat MCA by different mechanisms. ATP and ADP likely stimulate P2u and P2y purinoceptors, respectively.

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