Relaxation factor

Three years later Robert F Furchgott discov ered that the relaxing of smooth muscles such as blood vessel walls was stimulated by an unknown substance produced in the lining of the blood vessels (the endothelium) He called this substance the endothelium-dependent relaxing factor or EDRF and in 1986 showed that EDRF was NO Louis J Ignarro reached the same conclusion at about the same time Further support was provided by Salvador Moncada who showed that endothelial cells did in deed produce NO and that the l arginine to l citrulline conversion was responsible... 

Receptors linked to guanylyl cyclase and which catalyze the formation of guanosine triphosphate (GMP) to guanosine-3A -cychc monophosphate (cychc GMP) include those for atrial natriuretic factor (ANF) and endothehal-derived relaxing factor (EDRF), mediating vasodilatation, and nitric oxide [10102 3-9], NO, or a clearly related derivative. 

Because of round off errors, the Regula Falsa method should include a check for excessive iterations. A modified Regula Falsa method is based on the use of a relaxation factor, i.e., a number used to alter the results of one iteration before inserting into the next. (See the section on relaxation methods and Solution of Sets of Simultaneous Linear Equations. )... 

Relaxation methods may also be used to modify the value of an unknown before it is used in the next calculation. The effect of the relaxation factor X, may be seen in the following equation, where x " " is the value obtained at the present iteration. 

Furchgott and Zawadzki [1] first discovered that endothelial cells release a substance(s) responsible for the relaxation of vascular smooth muscle by acetylcholine this substance was named endothelium-derived relaxing factor (EDRF). This epoch-making discovery answers the question raised for nearly one hundred years by pharmacologists about why vascular smooth muscle is relaxed by acetylcholine, which however elicits contraction of the other smooth muscles. Because of its instability, the true chemical nature of EDRF was not easily identified. Several years later, several research groups independently found that the biological activities and biochemical properties of EDRF were identical... 

Endothelium-derived relaxing factor (nitric oxide)... 

The results of a number of studies demonstrate that the gas nitric oxide (NO) plays a functional role in the central nervous system. This all originated with the discovery that the so-called endothelium-derived relaxing factor (EDRF), found in blood vessels, and thought to be a peptide, was in fact NO. The potential roles of this freely diffusible gas have subsequently been extended to many other tissues and organs but we will concentrate on the possible neuronal roles of what is obviously a novel mediator. There are also suggestions that the closely related carbon monoxide may also have a function in the central nervous system. 

Chin, J.H., Azhar, S. and Hoffman, B.B. (1992). Inactivation of endothelial derived relaxing factor by oxidized lipoproteins. 

Ignarro, L.J. (1990). Biosynthesis and metabolism of endothelium-derived relaxation factor. Ann. Rev. Pharmacol. Toxicol. 30, 535-560. 

Moncada, S., Radomski, M.W. and Palmer, R.M. (1988). Endothelium-derived relaxing factor identification as nitric oxide and role in the control of vascular tone and platelet function. Biochem. Pharmacol. 37, 2495-2501. 

A relationship between polyol pathway activity and reduction in endothelium-dependent relaxation in aorta from chronic STZ-diabetic rats has recently been reported (Cameron and Cotter, 1992). In agreement with several previous studies (Oyama et al., 1986 Kamata et al., 1989), endothelial-dependent relaxation was defective in the diabetic rats but the deficit was prevented by prior treatment with an AR inhibitor. The mechanism underlying the defect has been speculated to be due to decreased production of endothelium-derived relaxing factor (EDRF) or nitric oxide, NO (Hattori et al., 1991). It has been speculated that these vascular abnormalities may lead to diminished blood flow in susceptible tissues and contribute to the development of some diabetic complications. NO is synthesized from the amino-acid L-arginine by a calcium-dependent NO synthase, which requires NADPH as a cofactor. Competition for NADPH from the polyol pathway would take place during times of sustained hyperglycaemia and... 

Gryglewski, R.J., Palmer, R.M.J. and Moncada, S. (1986). Superoxide anion is involved in the breakdown of endothelium-derived relaxing factor. Nature 320, 454—456. 

ED35 Eflective dose producing 35% maximum response EDso Effective dose producing 50% maximum response EDF Eosinophil differentiation 6ctor EDL Extensor digitorum longus EDN Eosinophil-derived neurotoxin EDRF Endothelium-derived relaxing factor... 

First described in the 1980s as "endothelium-derived relaxing factor," nitric oxide (NO) is a vasodilator believed to play a role in regulation of blood pressure under physiologic and pathophysiological conditions. For example, inhibition of NO synthesis under normal conditions and during septic shock results in a significant elevation of blood pressure. 

L.J. Ignarro, G.M. Buga, K.S. Wood, R.E. Byrns, and G. Chaudhuri, Endothelium-derived relaxing factor produced and released from artery and vein is nitric-oxide. Proc. Natl. Acad. Sci. U.S.A. 84, 9265-9269 (1987). 

T. Akaike, M. Yoshida,Y. Miyamoto, K. Sato, M. Kohno, K. Sasamoto, K. Miyazaki, S. Ueda, and H. Maeda, Antagonistic action of imidazolineoxyl N-oxides against endothelium-derived relaxing factor. NO through a radical reaction. Biochemistry 32, 827-832 (1993). 

A. Wennmalm, B. Lanne, and A.S. Petersson, Detection of endothelial-derived relaxing factor in human plasma in die basal state and following ischemia using electron-paramagnetic resonance spectrometry. Anal. Biochem. 187, 359-363 (1990). 

The discretized equations of the finite volume method are solved through an iterative process. This can sometimes have difficulty converging, especially when the nonlinear terms play a strong role or when turbulence-related quantities such as k and s are changing rapidly, such as near a solid surface. To assist in convergence a relaxation factor can be introduced ... 

P2Y receptors that are found on endothelial cells elicit a Ca2+-dependent release of endothelium-dependent relaxing factor (EDRF) and vasodilation. A secondary activation of a Ca2+-sensitive phospholipase A2 increases the synthesis of endothelial prostacyclin, which limits the extent of intravascular platelet aggregation following vascular damage and platelet stimulation. The P2Y-mediated vasodilation opposes a vasoconstriction evoked by P2X receptors located on vascular smooth muscle cells. The latter elicit an endothelial-independent excitation (i.e. constriction). P2Y receptors are also found on adrenal chromaffin cells and platelets, where they modulate catecholamine release and aggregation respectively. 

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