Il-6 impairs endothelium-dependent NO-cGMP-mediated relaxation and enhances contraction in systemic vessels of pregnant rats

"Orshal, J. M. and Khalil, R. A. (2004). Interleukin-6 impairs endothelium-dependent no-cgmp-mediated relaxation and enhances contraction in systemic vessels of pregnant rats. Am J Physiol Regul Integr Comp Physiol, 286(6):R1013-1023."


Read more: CiteULike: Interleukin-6 impairs endothelium-dependent NO-cGMP-mediated relaxation and enhances contraction in systemic vessels of pregnant rats:

Ghrelin Provides Positive Metabolic Effects Through Nitric Oxide Regulation.

"ghrelin plays a significant role in the regulation of glucose homeostasis, lipid profiles and body composition. Importantly, ghrelin has antinflammatory and antiapoptotic effects both in vivo and in vitro."

Note: Some of its action is achieved through signalling via NO/cGMP. Excess production of ammonia such as those from bacteria may influence the regulation of this protein.

CiteULike: Cardiovascular and Metabolic Effects of Ghrelin.: "Tesauro, M., Schinzari, F., Caramanti, M., Lauro, R., and Cardillo, C. (2010). Cardiovascular and metabolic effects of ghrelin. Current diabetes reviews."

Reduced NO-cGMP Signaling Contributes to Vascular Inflammation and Insulin Resistance Induced by High-Fat Feeding

Reduced signaling via the NO-cGMP pathway is a mediator of vascular inflammation and insulin resistance during overnutrition induced by high-fat feeding. Therefore, phosphodiesterase-5, soluble guanylyl cyclase, and other molecules in the NO-cGMP pathway (eg, protein kinase G) constitute potential targets for the treatment of vascular dysfunction in the setting of obesity.

CiteULike: Reduced NO-cGMP Signaling Contributes to Vascular Inflammation and Insulin Resistance Induced by High-Fat Feeding: "Rizzo, N. O., Maloney, E., Pham, M., Luttrell, I., Wessells, H., Tateya, S., Daum, G., Handa, P., Schwartz, M. W., and Kim, F. (2010). Reduced no-cgmp signaling contributes to vascular inflammation and insulin resistance induced by high-fat feeding. Arterioscler Thromb Vasc Biol, 30(4):758-765."

NO-cGMP and Mitochondrial Biogenesis -- Mediator of PGC-1a

As we have noted, hyperammonia may impair the NO-cGMP pathway. Nisoli explains, "nitric oxide-cGMP-dependent pathway controls mitochondrial biogenesis and body energy balance."

Nisoli, E., Clementi, E., Paolucci, C., Cozzi, V., Tonello, C., Sciorati, C., Bracale, R., Valerio, A., Francolini, M., Moncada, S., and Carruba, M. O. (2003). Mitochondrial biogenesis in mammals: the role of endogenous nitric oxide. Science (New York, N.Y.), 299(5608):896-899. http://www.citeulike.org/user/HEIRS/article/7030900





HEIRS Environmental Illness Research Blog: Dysfunction of Methylation and Nrf2 in Environmental Illness - A Better Explanation than NO/ONOO- ?

Downregulation of the Ornithine System, the Heart and NO-cGMP!

Hypertrophy of cardiomyocytes was induced by AngII, this caused an increase in putrescine, spermidine and total polyamine pool in association with a decreased level of NO. Expressions of eNOS and PKG-I were down-regulated, [Ca2+]i was increased, and expressions of c-Fos and c-Myc upregulated. DFMO reversed these changes induced by AngII.

Lin, Y., Liu, J.-C., Zhang, X.-J., Li, G.-W., Wang, L.-N., Xi, Y.-H., Li, H.-Z., Zhao, Y.-J., and Xu, C.-Q. (2010). Downregulation of the ornithine decarboxylase/polyamine system inhibits angiotensin-induced hypertrophy of cardiomyocytes through the no/cgmp-dependent protein kinase type-i pathway. Cellular Physiology and Biochemistry, 25(4-5).





HEIRS Environmental Illness Research Blog: Dysfunction of Methylation and Nrf2 in Environmental Illness - A Better Explanation than NO/ONOO- ?