General physiology: receptor desensitisation: practice question

A Physiology question in the style of the NEET PG paper. Answer it first, then read why the right option is right and why each of the others is wrong.

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Physiology · General physiology: receptor desensitisation

Sample item

A patient with asthma on regular high-dose salbutamol finds the bronchodilator response gradually weakening although the dose is unchanged. Which cellular mechanism best explains this?

AReceptor phosphorylation followed by arrestin binding, uncoupling it from GsBRapid hydrolysis of salbutamol by plasma esterasesCGreater cAMP breakdown because Gi is activated by salbutamolDIncreased synthesis of beta receptors saturating the response

Original practice item, not a recalled exam question. Nothing here is recorded.

The answer and the reasoning

A. Receptor phosphorylation followed by arrestin binding, uncoupling it from Gs

Prolonged agonist exposure leads to phosphorylation of the receptor by G-protein-coupled receptor kinases. Beta-arrestin then binds, uncouples the receptor from Gs and promotes internalisation, so the same dose gives a smaller response (tachyphylaxis).

Option by option

A. Receptor phosphorylation followed by arrestin binding, uncoupling it from Gs (correct)
Correct. Phosphorylation and arrestin binding uncouple the receptor from Gs.
B. Rapid hydrolysis of salbutamol by plasma esterases
Salbutamol is not inactivated by plasma esterases, and the dose-independent loss points to receptor change.
C. Greater cAMP breakdown because Gi is activated by salbutamol
Salbutamol acts on Gs-coupled receptors and does not activate Gi.
D. Increased synthesis of beta receptors saturating the response
Receptor number tends to fall with prolonged exposure, not rise.

Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.

Questions about this Physiology question

What is the answer to this Physiology question?

The best answer is A, Receptor phosphorylation followed by arrestin binding, uncoupling it from Gs. Prolonged agonist exposure leads to phosphorylation of the receptor by G-protein-coupled receptor kinases.

Why is "Rapid hydrolysis of salbutamol by plasma esterases" not the answer?

Salbutamol is not inactivated by plasma esterases, and the dose-independent loss points to receptor change.

Why is "Greater cAMP breakdown because Gi is activated by salbutamol" not the answer?

Salbutamol acts on Gs-coupled receptors and does not activate Gi.

Why is "Increased synthesis of beta receptors saturating the response" not the answer?

Receptor number tends to fall with prolonged exposure, not rise.

What concept does this question test?

It tests General physiology: receptor desensitisation in Physiology. Beta-arrestin then binds, uncouples the receptor from Gs and promotes internalisation, so the same dose gives a smaller response (tachyphylaxis).

How hard is this question?

We tag it as an application question: it asks you to use a fact on a patient or a finding. The tag is our own editorial judgement, not an official difficulty rating, so read the reason for every option, not only the answer.

How should I study General physiology: receptor desensitisation?

For each system, sketch the key graph (pressure–volume loop, oxygen dissociation curve, nephron handling) and explain it aloud. Then use the flashcards and the other Physiology questions on this site to test what stuck.

Is this a real NEET PG question?

No. It is an original practice item (editorial status: sample, version 1). NextPrep does not publish recalled or leaked questions, and independent faculty review of this item has not been completed yet, so confirm important facts in a standard textbook.