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 results in smooth muscle relaxation. This signaling mechanism is illustrated below:
Research published by Gustafsson, Persson, and Moncada (1990) found that nitric oxide production in the lungs decreases immediately under acute hypoxia (low oxygen), which causes the pulmonary blood vessels to constrict. This, in turn, limits oxygen delivery to the lungs, heart, red blood cells and mitochondria. A study published in the journal Nature (Beall et al. 2001) examined chronically hypoxic, high altitude populations of Tibetans and Bolivian Aymara, two countries almost halfway across the world from one other, and found that exhaled levels of Nitric oxide were unusually high relative to a low-altitude reference sample from the United States.
What is a likely conclusion that can be made with these findings?