Vasorelaxant activity of some oxime derivatives
Language English Country Netherlands Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
17706962
DOI
10.1016/j.ejphar.2007.07.040
PII: S0014-2999(07)00816-3
Knihovny.cz E-resources
- MeSH
- Aorta drug effects physiology MeSH
- Hydrophobic and Hydrophilic Interactions MeSH
- Enzyme Inhibitors pharmacology MeSH
- Blood Pressure drug effects physiology MeSH
- Rats MeSH
- Hydroxamic Acids pharmacology MeSH
- NG-Nitroarginine Methyl Ester pharmacology MeSH
- Nitric Oxide physiology MeSH
- Oximes pharmacology MeSH
- Pentolinium Tartrate pharmacology MeSH
- Rats, Wistar MeSH
- Vasodilation drug effects physiology MeSH
- Vasodilator Agents pharmacology MeSH
- Dose-Response Relationship, Drug MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- acetaldehyde oxime MeSH Browser
- acetohydroxamic acid MeSH Browser
- formaldoxime MeSH Browser
- Enzyme Inhibitors MeSH
- Hydroxamic Acids MeSH
- NG-Nitroarginine Methyl Ester MeSH
- Nitric Oxide MeSH
- Oximes MeSH
- Pentolinium Tartrate MeSH
- Vasodilator Agents MeSH
Several non-aromatic substituted oxime derivatives (formamidoxime, acetaldoxime, acetone oxime, acetohydroxamic acid, formaldoxime) function as vasorelaxant NO donors when added to precontracted aortic rings in vitro. This study was aimed to evaluate whether these substances posses vasodilator properties under in vivo conditions. We studied blood pressure changes elicited by administration of these compounds to conscious chronically catheterized Wistar rats in which endogenous NO synthesis was acutely inhibited by N(omega)-nitro-L-arginine methyl ester (L-NAME) pretreatment (30 mg/kg i.v.). Three of the tested substances (formaldoxime, acetohydroxamic acid and formamidoxime) induced pronounced dose-dependent blood pressure reduction which was further augmented when baroreflex operation was interrupted by ganglionic blockade (5 mg/kg pentolinium). Pretreatment of rats with methylene blue (soluble guanylate cyclase inhibitor) was used to estimate the contribution of NO to observed blood pressure lowering effects of the above compounds. Nitric oxide seems to be responsible for the entire formaldoxime-induced blood pressure decrease and for a considerable part of blood pressure changes elicited by formamidoxime. On the contrary, we did not find a significant NO contribution to blood pressure reduction caused by acetohydroxamic acid. In conclusion, our study confirmed in vivo vasodilator effects of three above mentioned compounds which were earlier demonstrated to induce in vitro vasorelaxation. It indicated a variable contribution of nitric oxide to blood pressure changes elicited by particular compounds. Substances with hydrophilic character (formamidoxime, acetohydroxamic acid, formaldoxime) were effective, whereas less hydrophilic substance (acetaldoxime) or slightly hydrophobic one (acetone oxime) were ineffective.
References provided by Crossref.org
Altered Balance between Vasoconstrictor and Vasodilator Systems in Experimental Hypertension
