Results of Experiment 1 and Analysis

For further evidence, the two scientists raised rat offsprings in a 10% oxygen environment. Because oxygen sensing is done within protein and potassium channels in organisms as well, the scientists found out that there were signs of blunted and reduced hypoxic ventilatory response. The potassium channel sensors failed to recognize the Hypoxic conditions. (Teppema and Dahan 2010, p 686) This strongly suggests the innate viability of the Hypoxic Drive to function fully within organisms. It displays that through natural selection and acclimatization of organisms to the environment, the Hypoxic Drive is left undeveloped within organisms at first, allowing Carbon Dioxide sensation to be active from the start. This vastly helps “hatch the egg” to see the answer as to why the Hypoxic Drive is a secondary respiratory drive in humans. The experimental reports relay that the carotid bodies of rats contained the ability to open and close potassium channels. It is known that potassium serves to increase perfusion and also help the electrical network of organism’s bodies. (McCutcheon, p 340-341) Teppema and Dahan noted that the channels were inactive in an environment where there were low peripheral oxygen levels. The Hypoxic Drive did not regulate so the Potassium levels remained minimal. However, when there was interaction with carbon dioxide, the Potassium channels were able to transport potassium ions through the channels. This suggests that the Hypoxic Drive is not integrated well within the body contributing to the minimalized aid it provides to the body compared to carbon dioxide regulation.


Above is a sample picture of the primary potassium channels used to 
infuse and control cellular disposition and permeability to potassium ions.