New insights into the role of nitric oxide in cardiovascular protection (part 11). CONCLUSIONS
In summary, cAMP levels regulated by PDE4 and PDE2 may up-regulate the nitric oxide-cGMP pathway in endothelial cells. Conversely, in smooth muscle cells cGMP (related to nitric oxide) may down-regulate PDE3 and therefore potentiate the effect of PDE4 inhibition. Reciprocal interactions between cAMP and cGMP are favoured by nitric oxide in endothelial cells, as in vascular smooth muscle cells. Taken together these results support the hypothesis that cGMP (related to nitric oxide production) enhances cAMP-mediated relaxation via the inhibition of PDE3. Glad you are finally going to spend less time and money shopping for the treatment you need? Our will be glad to give you that and a lot more when you become a customer, because health is very important to us.
These results show that cardiac nitric oxide and iron-nitric oxide adduct formation is enhanced during ischemia by pretreatment of rats with a cardioprotective dose of LPS; and that the mechanisms of nitric oxide-induced vasodilation involve complex interaction between cGMP and cAMP metabolic pathways, in which PDEs probably play an important role. The contribution of vasodilation and inhibition of platelet aggregation remains to be established. However, enhanced formation of nitric oxide and iron-nitric oxide ad-ducts in the myocardium during ischemia may cause vasodilation and restore an equilibrium between nitric oxide and oxygen-derived free radicals during reperfusion. The possible beneficial effect of enhanced endothelium nitric oxide production by cAMP-elevating cheap drugs requires further investigation.