Drugs that block the β-receptors for adrenaline and related compounds, generally known as catecholamines, in the heart are called β-blockers. These drugs are often used to treat heart disease. Sometimes β-blockers have a dual effect whereby they actually stimulate β-receptors if the levels of catecholamines in the body are low but exert their blocking effect if catecholamine levels are elevated, as they are often in patients with heart disease. Xamoterol is a β-blocker that has such a dual stimulation–inhibition effect. Before xamoterol can be most effectively used to treat heart disease, the level of body catecholamines at which the switch from a stimulating to a blocking effect occurs needs to be determined. Accordingly, Sato and coworkers* used exercise to stimulate catecholamine release in patients with heart disease. They measured a variety of variables related to the function of the cardiovascular system and related these variables to the level of the catecholamine norepinephrine in the blood with patients who did not exercise (group 1) and in three groups who engaged in increasing levels of exercise (groups 2–4), which increases the level of norepinephrine. Patients were randomly assigned to either no xamoterol (6 patients per group) or xamoterol (10 patients per group). Sato and his coworkers then related systolic blood pressure to the level of norepinephrine under the two conditions, drug and no drug. Is there any evidence that xamoterol had an effect, compared to control? At what level of plasma norepinephrine does xamoterol appear to switch its action from a mild βstimulant to a β-blocker? Include a plot of the data in your analysis. B. Repeat your investigation of this problem using all of the data points listed in Table D-8, Appendix D. Do you reach the same conclusions? Why or why not? C. Which analysis is correct?
Table D-8
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