The Influence of Ammonium Persulfate on Guinea Pig Tracheal Muscle Tone: Release of Nitric Oxide

This study was designed to further elucidate the role of the endothelium in regulation of cerebral vascular smooth muscle tone. Dose-dependent vasoconstrictive effects of serotonin (5-HT) were examined in endothelium-intact and endothelium-denuded ring segments prepared from canine basilar and middle cerebral arteries. Some preparations were pretreated with 10(-5) M N omega-nitro-L-arginine (L-NNA), an agent that inhibits the production of L-arginine-derived nitric oxide, one of the compounds proposed to be endothelium-derived relaxing factor. L-NNA alone elicited marked dose-dependent increases in tension in endothelium-intact preparations; a significantly smaller response was seen in endothelium-denuded preparations. The effects of L-NNA on endothelium-intact preparations were partially reversed by washing and treatment with L-arginine. The maximum tension induced by 5-HT was approximately doubled by removal of the endothelium as well as by L-NNA treatment of endothelium-intact preparations; a slight increase in maximum tension occurred in endothelium-denuded preparations treated with L-NNA. The concentration of 5-HT producing half-maximal contraction (ED50) was not affected by L-NNA. These data suggest that L-arginine-derived nitric oxide modulates canine cerebral arterial tone in both the resting state and during contraction with 5-HT.

Download Full-text

Ascending choline acetyltransferase and descending nitric oxide synthase immunoreactive neurones of the myenteric plexus project to the mucosa of the guinea pig gastric corpus

Neuroscience Letters ◽

10.1016/s0304-3940(97)00968-3 ◽

1998 ◽

Vol 241 (1) ◽

pp. 61-64 ◽

Cited By ~ 23

Author(s):

D Reiche ◽

M Schemann

Keyword(s):

Nitric Oxide ◽

Nitric Oxide Synthase ◽

Guinea Pig ◽

Choline Acetyltransferase ◽

Myenteric Plexus ◽

Gastric Corpus ◽

Oxide Synthase

Download Full-text

Inputs from intrinsic primary afferent neurons to nitric oxide synthase-immunoreactive neurons in the myenteric plexus of guinea pig ileum

Cell and Tissue Research ◽

10.1007/s004410050001 ◽

2000 ◽

Vol 299 (1) ◽

pp. 1-8 ◽

Cited By ~ 25

Author(s):

Z. S. Li ◽

J. B. Furness

Keyword(s):

Nitric Oxide ◽

Nitric Oxide Synthase ◽

Guinea Pig ◽

Myenteric Plexus ◽

Afferent Neurons ◽

Guinea Pig Ileum ◽

Primary Afferent Neurons ◽

Primary Afferent ◽

Oxide Synthase

Download Full-text

Inhibition of nitric oxide synthase prevents magnesium-free-induced epileptiform activity in guinea-pig piriform cortex neurones in vitro

Naunyn-Schmiedeberg s Archives of Pharmacology ◽

10.1007/pl00004968 ◽

1997 ◽

Vol 355 (4) ◽

pp. 452-456 ◽

Cited By ~ 8

Author(s):

V. Libri ◽

Rosamaria Santarelli ◽

Steven Nisticò ◽

Gian Battista Azzena

Keyword(s):

Nitric Oxide ◽

Nitric Oxide Synthase ◽

Guinea Pig ◽

Epileptiform Activity ◽

Piriform Cortex ◽

Oxide Synthase

Download Full-text

The Conversion of Methyl-2-Acetoxyethyl-2′-Chloroethylamine to an Acetylcholine-Like Aziridinium Ion and its Action on the Isolated Guinea Pig Ileum

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y72-116 ◽

1972 ◽

Vol 50 (8) ◽

pp. 798-808 ◽

Cited By ~ 14

Author(s):

M. Hirst ◽

C. H. Jackson

Keyword(s):

Aqueous Solution ◽

Guinea Pig ◽

Muscle Tone ◽

Recovery Period ◽

Induced Responses ◽

Agonist Activity ◽

Guinea Pig Ileum ◽

Aziridinium Ion ◽

Treatment Responses

Methyl-2-acetoxyethyl-2′-chloroethylamine (acetyicholine-mustard) isomerizes in aqueous solution to form a cyclic ion, N-methyl-N-(2-acetoxyethyl)aziridinium, which structurally resembles acetylcholine. It is a potent stimulant of the guinea pig ileum, being approximately one-sixth as potent as acetylcholine at pH 7.4 and one-third as potent at pH 8.4. The agonist activity is inhibited by atropine, by preincubation with acetylcholinesterase, and pretreatment with thiosulfate ion. Mepyramine does not inhibit the stimulant action.One hour exposures of ileum segments to concentrations of acetylcholine-mustard in excess of those producing maximal responses, followed by a 1 h recovery period, did not produce evidence of postsynaptic receptor alkylation. Post-treatment responses to acetylcholine were slightly depressed, but these reductions were not related to the incubation concentrations of the agonist haloalkylamine. Pilocarpine-induced responses were unaltered by this treatment whereas 5-hydroxytryptamine responses were slightly potentiated and histamine responses were slightly and inconsistently modified.These treatments produced persistent, dose-related increases in muscle tone, an effect consistent with accumulations of spontaneously liberated acetylcholine and possibly caused by inhibition of in situ acetylcholinesterase.Ostensibly, the evidence suggests that the acetylcholine-like aziridinium ion can stimulate, but not inhibit, the muscarinic receptors of the guinea pig ileum.

Download Full-text