Robert D. Furchgott’s Contribution To The Discovery Of Nitric Oxide As A Cardiovascular Signaling

1506 words - 6 pages

In 1998 the Nobel Prize in physiology was awarded to three scientists for their contribution to the discovery of nitric oxide (NO) as a physiological singling molecule, particularly in vascular smooth muscle: Dr. Robert F. Furchgott, Dr. Louis J. Ignarro, and Dr. Ferid Murad1,2. Although the Prize was only initially awarded to Furchgott and Murad, it was later admitted that without the work of Ignarro an important link would not have been made.
More specifically, in 1977 Murad found that nitric oxide was the active molecule causing vasodilation when studying the effects of vasodilatory effects nitroglycerine1,2. In 1980 when studying the effects of vasodilatory effects or acetylcholine in rabbit aorta, Furchgott found that vascular endothelial cells are necessary for vascular smooth muscle relaxation3. He concluded that endothelial cells produce what he called endothelium-derived relaxing factor (EDRF), a signaling molecule that caused vascular smooth muscle to relax1,3. Lastly, in 1986 Ignarro, showing that vascular endothelial cells produced similar responses when stimulated to produce EDRF and when exposed to NO, determined that nitric oxide and EDRF were the same molecule, thereby uniting the work of Murad and Furchgott into a cohesive vasodilatory model1,2.
Nitric Oxide and Vascular Relaxation
Nitric oxide is an abundant and diverse secondary signaling molecule throughout the body, playing roles in memory, learning, inflammation, and blood pressure. It is synthesized by nitric oxide synthase (NOS) from L-arginine and oxygen, though there are three known types of NOS: NOS 1, NOS 2 and NOS 34. NOS 1 and 3 are stimulated by high intracellular calcium ion concentrations, as caused by vasodilators like acetylcholine and bradykinin while NOS 2 is stimulated by cytokine activity4. Second and third type NOSs are found in immune cells and the nerve tissue respectively, whereas NOS1 is found primarily in endothelial tissue4. After being synthesized by NOS, NO is immediately released and acts quickly prior to being inactivated (for example, by hemoglobin), as it is a reactive free radical.
Vascular endothelial cells that are subjected to sheer stress or vasodilators (such as bradykinin and ADP) have resultantly high intracellular concentrations of calcium ions, leading to the activation of NOS1. NOS1 synthesizes NO from L-arginine and oxygen, then subsequently diffuses into surrounding vascular smooth muscle to directly activate guanylate cyclase4. Similarly, nitro-vasodilators such as nitroglycerin, as used by Murad, activate guanylate cyclase4. Guanylate cyclase converts GTP to 3,5-cGMP, which activates protein kinase G4. This then produces several general effects, including the opening of cellular calcium ion channels to increase intracellular concentration, culminating in myocyte relaxation (see Figure 1)4. The release of NO can also occur through increased blood flow (occurring from dilation of afferent...

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