By Harald H. H. W. Schmidt, Franz B. Hofmann, Johannes-Peter Stasch
After the invention of endogenous NO formation within the past due '80s and the 1998 Nobel Prize in body structure or medication, many researchers and physicians back took an interest within the NO/sGC interplay and cGMP-dependent signaling. This booklet is an enthusiastic party of cyclic guanosine monophosphate (cGMP) and amply illustrates the significance of this box of technology to sufferers and how during which the sphere has developed. it's solely dedicated to this fascinating and critical signaling molecule, addressing all fresh advances in figuring out guanylate cyclase legislation, NO/sGC interactions, cGMP effector mechanisms and their pathophysiological and pharmacological implications. specific realization can be given to medical functions of the unconventional cGMP-elevating medications that are at the horizon, hence spanning the continuum from simple technological know-how to health facility.
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Additional info for cGMP: Generators, Effectors and Therapeutic Implications
1998). In the following, results obtained with the NO-GC and NO-GC1 KO mice in cGMP relevant systems will be introduced and discussed. As the NO-GC2 KO was indistinguishable from WT mice except for the neuronal system, the results will not be mentioned separately. 3 Smooth Muscle Tone Role of NO-GC Isoforms in Vascular Smooth Muscle Although the important role of the NO/cGMP cascade in smooth muscle relaxation is well established and the NO-GC1 has been identified as the major NO receptor isoform, the distribution and function of the NO-GC isoforms in vasculature needs to be determined.
3 Smooth Muscle Tone Role of NO-GC Isoforms in Vascular Smooth Muscle Although the important role of the NO/cGMP cascade in smooth muscle relaxation is well established and the NO-GC1 has been identified as the major NO receptor isoform, the distribution and function of the NO-GC isoforms in vasculature needs to be determined. Analysis of the NO-GC receptor isoform content in aorta derived from the NO-stimulated cGMP-forming activities yielded approximately 94% and 6% for NO-GC1 and NO-GC2, respectively (Mergia et al.
NO was shown to be produced by the NO synthases (NOS) with the neuronal (nNOS or NOSI) and endothelial NOS (eNOS or NOSIII) being of major importance for the production of NO as a signalling molecule. In contrast, the high amounts of NO produced by the inducible NOS (iNOS or NOSII) exert direct toxic effects. KO mice deficient for either one of the NOSs exist, the respective phenotypes will be compared with those of the NO-GC deficient mice below. The available research data strongly suggest that most of the effects of NO as a signalling molecule are mediated by the activation of NO-GC; however, speculations on cGMP-independent physiological effects of NO are numerous.