Rinrada Kietadisorn

Publications of Rinrada Kietadisorn

• Tackling endothelial dysfunction by modulating NOS uncoupling: new insights into its pathogenesis and therapeutic possibilities.

  Authors: Rinrada Kietadisorn, Rio P Juni, An L Moens

  American journal of physiology. Endocrinology and metabolism. 12/2011; 302(5):E481-95.

  Endothelial nitric oxide synthase (eNOS) serves as a critical enzyme in maintaining vascular pressure by producing nitric oxide (NO); hence, it has a crucial role in the regulation of endothelialEndothelial nitric oxide synthase (eNOS) serves as a critical enzyme in maintaining vascular pressure by producing nitric oxide (NO); hence, it has a crucial role in the regulation of endothelial function. The bioavailability of eNOS-derived NO is crucial for this function and might be affected at multiple levels. Uncoupling of eNOS, with subsequently less NO and more superoxide generation, is one of the major underlying causes of endothelial dysfunction found in atherosclerosis, diabetes, hypertension, cigarette smoking, hyperhomocysteinemia, and ischemia/reperfusion injury. Therefore, modulating eNOS uncoupling by stabilizing eNOS activity, enhancing its substrate, cofactors, and transcription, and reversing uncoupled eNOS are attractive therapeutic approaches to improve endothelial function. This review provides an extensive overview of the important role of eNOS uncoupling in the pathogenesis of endothelial dysfunction and the potential therapeutic interventions to modulate eNOS for tackling endothelial dysfunction.

• Role of tetrahydrobiopterin (BH4) in hyperhomocysteinemia-induced endothelial dysfuction: new indication for this orphan-drug?

  Authors: Rinrada Kietadisorn, Bas L Kietselaer, Harald H H W Schmidt, An L Moens

  American journal of physiology. Endocrinology and metabolism. 03/2011; 300(6):E1176; author reply E1177-8.

  n/a.

• Targeting endothelial and myocardial dysfunction with tetrahydrobiopterin.

  Authors: An L Moens, Rinrada Kietadisorn, Judy Y Lin, David Kass

  Journal of molecular and cellular cardiology. 03/2011; 51(4):559-63.

  Tetrahydrobiopterin (BH(4)) is an essential cofactor for aromatic amino acid hydroxylases and for all three nitric oxide synthase (NOS) isoforms. It also has a protective role in the cell as anTetrahydrobiopterin (BH(4)) is an essential cofactor for aromatic amino acid hydroxylases and for all three nitric oxide synthase (NOS) isoforms. It also has a protective role in the cell as an antioxidant and scavenger of reactive nitrogen and oxygen species. Experimental studies in humans and animals demonstrate that decreased BH(4)-bioavailability, with subsequent uncoupling of endothelial NOS (eNOS) plays an important role in the pathogenesis of endothelial dysfunction, hypertension, ischemia-reperfusion injury, and pathologic cardiac remodeling. Synthetic BH(4) is clinically approved for the treatment of phenylketonuria, and experimental studies support its capacity for ameliorating cardiovascular pathophysiologies. To date, however, the translation of these studies to human patients remains limited, and early results have been mixed. In this review, we discuss the pathophysiologic role of decreased BH(4) bioavailability, molecular mechanisms regulating its metabolism, and its potential therapeutic use as well as pitfalls as an NOS-modulating drug. This article is part of a special issue entitled ''Key Signaling Molecules in Hypertrophy and Heart Failure.''

• Folic Acid as a cardiovascular drug: dose matters.

  Authors: Rinrada Kietadisorn, Harald H Schmidt, An L Moens

  The American journal of cardiology. 12/2010; 106(11):1673-4.