Noradrenaline (NA, 10 μg/kg) is injected into an anaesthetised rat and effects on arterial blood pressure (ABP, top panel) and heart rate (HR, bottom panel) are shown below. Which of the following antagonists would MOST LIKELY prevent the effect on HR?

Question

BlackTom AI · Accepted Answer

Noradrenaline raises arterial pressure mainly by alpha1-mediated vasoconstriction; the baroreceptor reflex then increases vagal (parasympathetic) outflow to slow the heart via muscarinic (M2) receptors. In the trace the top panel (ABP) shows a clear transient rise after NA, and the bottom panel (HR) shows a simultaneous decrease in heart rate — a classic reflex bradycardia.

1. Relevant concepts:
- Noradrenaline (NA) acts on vascular alpha1 → vasoconstriction → increased ABP.
- Baroreceptor reflex: increased arterial pressure → increased carotid/aortic baroreceptor firing → NTS → increased vagal efferent and decreased sympathetic efferent activity to the heart.
- Vagal slowing of heart rate is mediated by M2 muscarinic receptors on the sinoatrial node; atropine is a muscarinic antagonist that blocks this effect.

2. Step-by-step reasoning:
- Injection of NA (10 μg/kg) causes alpha1-mediated vasoconstriction → ABP rises (observed).
- The rise in ABP is sensed by baroreceptors, triggering reflex arcs that increase parasympathetic (vagal) output and reduce sympathetic output to the heart.
- Increased vagal activity releases acetylcholine at the SA node, activating M2 receptors and causing bradycardia (observed HR fall).
- If muscarinic receptors are blocked, the vagally mediated bradycardia cannot occur, so the HR effect would be prevented.

3. Calculations: (no numeric algebra required) Temporal correlation in the trace shows ABP rise followed immediately by HR fall, supporting reflex mechanism rather than direct beta1 effect dominating.

4. Why the correct answer is correct:
Atropine blocks cardiac muscarinic receptors, preventing vagally mediated slowing of the heart produced by the baroreceptor reflex after NA-induced hypertension; therefore it most likely abolishes the HR decrease.

5. Why other options are incorrect:
- Propranolol (beta blocker) would block beta1-mediated tachycardia but does not block vagal M2 receptors; it would not prevent a vagal-induced bradycardia and might even permit greater bradycardia.
- Losartan (AT1 antagonist) and captopril (ACE inhibitor) act on the renin–angiotensin system, not on acute reflex vagal pathways.
- Clonidine is a central alpha2 agonist (reduces sympathetic outflow) and would not acutely block the vagal muscarinic effect.

Conclusion: The most likely antagonist to prevent the HR effect is a muscarinic blocker — atropine (answer a), which matches the provided answer.

Noradrenaline (NA, 10 μg/kg) is injected into an anaesthetised rat and effects on arterial blood pressure (ABP, top panel) and heart rate (HR, bottom panel) are shown below. Which of the following antagonists would MOST LIKELY prevent the effect on HR?单项选择题

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