In mammals, including humans, nitric oxide (NO) is an important cellular signaling molecule involved in many physiological processes. Research into its function led to the 1998 Nobel Prize for discovering its role in cardiovascular function. One specific role of nitric oxide in cardiac function is the dilation of blood vessels, a process called vasodilation. Vasodilation of the arteries lowers blood pressure and decreases the force that the heart muscle needs to exert to pump blood.
The cell signaling mechanism begins when NO diffuses into the smooth muscle cells of the blood vessel and activates guanylyl cyclase. The complete signaling mechanism is illustrated in Figure 1 above:
Fig. 1: Signaling cascade of Nitric oxide involving cyclic GMP (guanosine monophosphate), guanosine triphosphate (GTP), Protein Kinase G, calcium ions (Ca2+), and PDE (phosphodiesterase).
In addition to its role as a vasodilator, NO is produced by macrophages, phagocytic cells of the immune system. Macrophages use NO to counteract DNA replication in infectious microorganisms and they produce compounds called peroxynitrites that are toxic to many bacteria and fungi. Some infections can result in a medical condition known as septic shock, which can be fatal. The main characteristic of septic shock is a dangerous lowering of blood pressure, which impairs blood flow at the microscopic level of the capillaries (smallest blood vessels), resulting in hypoxic (low oxygen) conditions in tissues and cells.
What is a possible cause for the symptoms of septic shock?
In mammals, including humans, nitric oxide (NO) is an important cellular signaling molecule involved in many physiological processes. Research into its function led to the 1998 Nobel Prize for discovering its role in cardiovascular function. One specific role of nitric oxide in cardiac function is the dilation of blood vessels, a process called vasodilation. Vasodilation of the arteries lowers blood pressure and decreases the force that the heart muscle needs to exert to pump blood.
The cell signaling mechanism begins when NO diffuses into the smooth muscle cells of the blood vessel and activates guanylyl cyclase. The complete signaling mechanism is illustrated in Figure 1 above:
Fig. 1: Signaling cascade of Nitric oxide involving cyclic GMP (guanosine monophosphate), guanosine triphosphate (GTP), Protein Kinase G, calcium ions (Ca2+), and PDE (phosphodiesterase).
In addition to its role as a vasodilator, NO is produced by macrophages, phagocytic cells of the immune system. Macrophages use NO to counteract DNA replication in infectious microorganisms and they produce compounds called peroxynitrites that are toxic to many bacteria and fungi. Some infections can result in a medical condition known as septic shock, which can be fatal. The main characteristic of septic shock is a dangerous lowering of blood pressure, which impairs blood flow at the microscopic level of the capillaries (smallest blood vessels), resulting in hypoxic (low oxygen) conditions in tissues and cells.
What is a possible cause for the symptoms of septic shock?
The correct option is D Increased amounts of NO released by macrophages during an infection can cause extreme vasodilation, leading to a drop in blood pressure and impaired oxygen delivery to body cells and tissues.
- When excessive of NO is released into the bloodstream by the macrophages to kill or restrict the growth of pathogens.
- It can cause excessive vasodilation preventing oxygen from reaching the vital organs, impairing their function and in extreme conditions may cause death.
So, the correct answer is 'Increased amounts of NO released by macrophages during an infection can cause extreme vasodilation, leading to a drop in blood pressure and impaired oxygen delivery to body cells and tissues'
- When excessive of NO is released into the bloodstream by the macrophages to kill or restrict the growth of pathogens.
- It can cause excessive vasodilation preventing oxygen from reaching the vital organs, impairing their function and in extreme conditions may cause death.
