Limited access

Upgrade to access all content for this subject

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 below:

Figure 1. Signaling cascade of Nitric oxide signal involving cyclic GMP (guanosine monophosphate), guanosine triphosphate (GTP), Protein Kinase G, calcium ions ($Ca^{2+}$) and PDE (phosphodiesterase). Gray Mitchell, C. Created for Copyright 2016. All rights reserved.

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.

Which of the following 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 $NO$?


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


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


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

Select an assignment template