ArticleBritish journal of pharmacology1999
Nitric oxide synthase inhibition by dimaprit and dimaprit analogues.
Article in British journal of pharmacology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 6 citations in OpenAlex.
- Acute Intestinal Inflammation Depletes/Recruits Histamine-Expressing Myeloid Cells From the Bone Marrow Leading to Exhaustion of MB-HSCs.Cellular and molecular gastroenterology and hepatology · 2021Article
- Multi-targeted mechanisms underlying the endothelial protective effects of the diabetic-safe sweetener erythritol.PloS one · 2013Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. The similarity in molecular structure between the histamine H2-agonist dimaprit (3-dimethylamino-propyl-isothiourea) and the endogenous nitric oxide synthase (NOS) substrate L-arginine prompted us to study the effect of dimaprit and some dimaprit analogues on NOS activity. Dimaprit and some of its analogues were tested in an in vitro assay which measures the conversion of [3H]-L-arginine to [3H]-L-citrulline. Dimaprit inhibits rat brain NOS (nNOS) concentration dependently with an IC50 of 49+/-14 microM. 2. Removal of one or both of the methyl groups from the non-isothiourea nitrogen of dimaprit improved nNOS inhibitory properties. Aminopropylisothiourea is the most potent compound (IC50 = 4.1+/-0.9 microM) of the series followed by methylaminopropylisothiourea (IC50 = 7.6 +/- microM). 3. The observed effect of aminopropylisothiourea and methylaminopropyl-isothiourea are probably not due to the compounds themselves but to the corresponding mercaptoalkylguanidines, rearrangement products formed in aqueous solutions. This hypothesis is strengthened by the finding that aminobutylisothiourea is not active since a rearrangement to mercaptobutylguanidine does not occur. 4. Remarkably, nitrosylation of the isothiourea group of dimaprit decreases nNOS inhibitory activity, while nitrosylation of the guanidine analogue of dimaprit increases the inhibition of nNOS activity. 5. The pharmacological profile of dimaprit includes inhibition of nNOS. The nNOS inhibitory activity occurs in the same concentration range as the H2-agonist and H3-agonist activity of this compound.
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