Inhibition of aldehyde dehydrogenase type 2 attenuates vasodilatory action of nitroglycerin in human veins

Author:

Huellner Martin W.1,Schrepfer Sonja2,Weyand Michael3,Weiner Henry4,Wimplinger Isabella5,Eschenhagen Thomas1,Rau Thomas1

Affiliation:

1. Institute of Experimental and Clinical PharmacologyUniversity Medical Center Hamburg-EppendorfHamburg-EppendorfGermany

2. Department of Cardiovascular SurgeryUniversity Medical Center Hamburg-EppendorfHamburg-EppendorfGermany

3. Department of Cardiovascular SurgeryFriedrich-Alexander UniversityErlangen-NürnbergGermany

4. Department of BiochemistryPurdue UniversityWest Lafayette IndianaUSA

5. Institute of Human GeneticsUniversity Medical Center Hamburg-EppendorfHamburg-EppendorfGermany

Publisher

Wiley

Subject

Genetics,Molecular Biology,Biochemistry,Biotechnology

Reference40 articles.

1. Guanylate cyclase: activation by azide, nitro com pounds, nitric oxide, and hydroxyl radical and inhibition by hemoglobin and myoglobin;Murad F.;Adv. Cyclic Nucl. Res.,1978

2. Mechanism of vascular smooth muscle relaxation by organic nitrates, nitrites, nitroprusside and nitric oxide: evidence for the involvement of S-nitrosothiols as active intermediates;Ignarro L. J.;J. Pharma col. Exp. Therapeut.,1981

3. Endothelium-derived relaxing factor produced and released from artery and vein is nitric oxide.

4. Nitric oxide release accounts for the biological activity of endothelium-derived relaxing factor

5. The obligatory role of endothelial cells in the relaxation of arterial smooth muscle by acetylcholine

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