By Rodney A. Rhoades PhD, David R. Bell PhD
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Example text
Therapeutic agents for angina pectoris (severe chest pain resulting from insufficient blood supply to cardiovascular tissues) generally included the administration of nitrates, a commonly used agent that reduces myocardial oxygen demand. Nitrates act as an exogenous source of nitric oxide (NO), which can stimulate soluble GCs and increase cellular levels of cGMP. Formation of cGMP transduces a signal that promotes relaxation of vascular smooth muscle in arteries and veins. Nitrates’ salutary effect in treating myocardial ischemia is to dilate veins, which allows blood to translocate from inside the ventricles into the peripheral tissues.
HO oxidation of heme results in the production of CO and biliverdin (responsible for the green color of bruises). Although it is a weak activator of sGC, HOderived CO is thought to have a role in neuronal signaling, including olfactory transmission, vascular tone, and platelet aggregation to name a few physiologic processes. CO can also modulate MAPK activity, and the numerous signaling pathways regulated by these signaling molecules extend CO a role in proliferation, inflammation, and cell death.
Key to the apoptotic program is absence of release of toxic cellular products into the surrounding tissue space. This distinguishes apoptotic or programmed cell death from necrosis. Necrotic cell death usually results from acute injury to cells, and in response the cells rupture and release their contents on neighboring cells, an event that can stimulate an inflammatory response and cause more damage. Not all cell death is pathologic. Over the course of a day, up to a million cells can die by apoptosis.
