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ient has a mutation in the gene coding for a cardiac cell’s \\(\\beta_1…

Question

ient has a mutation in the gene coding for a cardiac cell’s \\(\beta_1\\)-adrenergic ptor. the mutation alters the region of the receptor that normally binds its cellular g protein. the receptor still sits on the membrane and can bind ephrine, but the heart shows almost no increase in rate or contractility during pathetic stimulation. ich explanation best accounts for this clinical outcome? the receptor works normally, but epinephrine becomes nonpolar during sympathetic activity and cannot attach to the membrane receptor. the g protein is unnecessary in cardiac cells because epinephrine normally diffuses directly into the cytoplasm to increase heart rate. the receptor can still activate the g protein because binding epinephrine automatically triggers intracellular signaling even without a proper receptor-g-protein connection. the receptor can bind epinephrine, but without proper interaction with its intracellular g protein, the signal cannot be transmitted into the cell, so the cardiovascular response does not occur.

Explanation:

Brief Explanations
  • Option 1: Epinephrine's polarity doesn't change during sympathetic activity, and it binds to membrane receptors, so this is incorrect.
  • Option 2: Epinephrine is a polar molecule and doesn't diffuse directly into cells; it acts via membrane receptors, so this is wrong.
  • Option 3: Receptor - G - protein interaction is crucial for signal transduction. Without proper interaction, intracellular signaling won't be triggered just by epinephrine binding, so this is incorrect.
  • Option 4: The receptor can bind epinephrine, but the mutation affects G - protein binding. Since G - protein is needed for signal transduction into the cell, without proper interaction, the signal isn't transmitted, and the cardiovascular response (increased heart rate/contractility) doesn't occur. This matches the clinical outcome.

Answer:

The receptor can bind epinephrine, but without proper interaction with its intracellular G protein, the signal cannot be transmitted into the cell, so the cardiovascular response does not occur.