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 signal involving cyclic GMP (guanosine monophosphate), guanosine triphosphate (GTP), Protein Kinase G, calcium ions ( $C a^{2 +}$ ) and PDE (phosphodiesterase).
In smooth muscle cells of the cardiovascular system, cyclic GMP is hydrolyzed by three types of phosphodiesterases, PDE1, PDE2, and PDE5. Research by Kass, Takimoto, Nagayama, and Champion (2007) found evidence that indicates patients with atherosclerosis (hardening and narrowing of the arteries) and congestive heart failure had elevated levels of PDE1 and PDE5.
What is a plausible scientific question that could have been posed by this research?

Do elevated levels of PDE 1 and PDE5 influence the signaling pathway of NO?

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Can PDE 1 and PDE5 inhibitors treat certain cardiovascular diseases by stimulating cGMP concentration in smooth muscle cells, resulting in arterial relaxation?

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Do elevated levels of PDE1 and PDE5 cause the rate of cGMP hydrolysis to decrease, resulting in atherosclerosis and congestive heart failure?

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Can elevated levels of PDE 1 and PDE5 cause certain cardiovascular diseases by increasing the levels of cGMP?

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Solution

The correct option is B Can PDE 1 and PDE5 inhibitors treat certain cardiovascular diseases by stimulating cGMP concentration in smooth muscle cells, resulting in arterial relaxation?
Administering PDE1 and PDE5 inhibitors will lead to the prevention of PDE (Phosphodiesterase) from converting cGMP to GMP,
cGMP is responsible for propelling the reaction in the forward direction, resulting in relaxation of the smooth muscles of the arteries, that lead to vasodialation
For a patient suffering from atherosclerosis, vasodialation does not occur due hardened arteries that contain depositions, where they also exhibit increased levels of PDE1 and PDE5
so, PDE1 and PDE5 inhibitors will bring down the levels of PDE1 and PDE5 in the smooth muscle cells, resulting in more amount of cGMP and possible relaxation of arterial muscle.
So, the correct answer is 'Can PDE 1 and PDE5 inhibitors treat certain cardiovascular diseases by stimulating cGMP concentration in smooth muscle cells, resulting in arterial relaxation?'

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C a^{2 +}

), and PDE (phosphodiesterase).
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Q. 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 Guanylate Cyclase which, in turn, stimulates the Guanylate Cyclase to generate cyclic GMP (guanosine monophosphate) from Guanosine Triphosphate (GTP). Protein Kinase G phosphorylates several proteins that regulate calcium concentrations and, in this case, causes alterations in thin and thick muscle filaments that result in smooth muscle relaxation. This signaling mechanism is illustrated below:
Signal transduction pathways are composed of a complex series of biochemical reactions but they can be described in three essential steps.
Which statement best identifies the role and sequence of the primary molecules involved in nitric oxide cell signaling?

Q. 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 Guanylate Cyclase which, in turn, stimulates the Guanylate Cyclase to generate cyclic GMP (guanosine monophosphate) from Guanosine Triphosphate (GTP). Protein Kinase G phosphorylates several proteins that regulate calcium concentrations and, in this case, causes alterations in thin and thick muscle filaments that result in smooth muscle relaxation. This signaling mechanism is illustrated above:
Signal transduction pathways are composed of a complex series of biochemical reactions and can be initiated two different ways.
Which statement best explains the primary function of each molecule involved in nitric oxide cell signaling?

C a^{2 +}

), and PDE (phosphodiesterase).
Nitroglycerin became famous in 1867 when Alfred Nobel patented an explosive mixture of nitroglycerin and diatomaceous earth as dynamite. Since then it has been widely used as a medication to treat the medical condition angina, which is chest pain caused by a lack of oxygen in the heart muscle and a common symptom of heart disease. Nitroglycerine is converted to nitric oxide by mitochondrial aldehyde dehydrogenase (Chen et al. 2007), which then functions as the signal in the NO transduction pathway. Unfortunately, patients quickly develop a tolerance to nitroglycerin and this prevents continuous administration.
Which of the following is NOT a plausible explanation for nitroglycerin tolerance in smooth muscle cells?

C a^{2 +}

), 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?

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