Final answer:
In heart failure, patients have increased levels of norepinephrine and epinephrine; however, their heart muscle becomes less responsive to these hormones due to receptor down regulation.
Step-by-step explanation:
In patients with heart failure, systemic levels of norepinephrine and epinephrine are increased, but the myocardium appears to be less responsive to the effect of these positive inotropic agents. This phenomenon is largely due to the down regulation of receptors on the heart muscle as a response to sustained high levels of these hormones. Epinephrine and norepinephrine, which are catecholamines released during sympathetic stimulation, normally bind to cardiac beta-1 receptors to increase heart rate and the force of contraction. However, in heart failure, chronic elevation of these catecholamines can lead to receptor desensitization and down regulation, making the myocardium less responsive to them, affecting both sympathetic and endocrine regulation of the cardiovascular system. This reduced sensitivity to catecholamines is an example of the body's adaptation to persistent high levels, but at the cost of reducing the positive inotropic (force-enhancing) and chronotropic (rate-enhancing) effects that would otherwise help the failing heart.