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This is a classic pharmacology experiment. Here are the answers:
1. Drug Used at Point X
Phentolamine (or phenoxybenzamine — a non-selective α-adrenergic receptor blocker)
This is the standard "Dale's vasomotor reversal" / "Epinephrine Reversal" experiment. The drug given at point X is an α-adrenergic blocker (classically phentolamine or phenoxybenzamine).
How to read the figure:
- Panel 1 (before X): Epinephrine (A) causes a BP rise; Norepinephrine (B) also causes a rise — both intact α responses.
- Panel 2 (point X): The α-blocker is administered. Notice a flat/depressed BP trace — basal BP falls.
- Panel 3 (after X): Epinephrine (A) now lowers BP (reversal!); Norepinephrine (B) still raises BP (only diminished, not reversed).
2. Type of Drug Interaction
Epinephrine Reversal (Dale's Vasomotor Reversal)
This is a pharmacodynamic drug interaction — specifically receptor-level antagonism (competitive or non-competitive blockade):
| Feature | Explanation |
|---|---|
| Mechanism | α-blocker blocks α₁ receptors on vascular smooth muscle |
| Epinephrine after α-block | α₁ vasoconstriction is blocked; unmasked β₂ vasodilation causes BP to fall (reversal) |
| Norepinephrine after α-block | Not reversed — only diminished, because NE has negligible β₂ vasodilatory activity |
| Isoproterenol (pure β agonist) | Would be unaffected by the α-blocker |
The interaction is pharmacodynamic antagonism at the receptor level — the α-blocker selectively removes the pressor (α₁) component of epinephrine, leaving the depressor (β₂) component unopposed, reversing the net BP effect.
Source: Katzung's Basic and Clinical Pharmacology, 16th Ed. (Figure 10-3); Lippincott Illustrated Reviews Pharmacology, p. 254–255
No any 3rd panel
Looking at the image again carefully:
The figure has only 2 panels separated by point X:
- Panel 1 (left): Epinephrine (A) and Norepinephrine (B) given → both cause BP rise (peaks visible around 160 mmHg)
- Point X: Drug is administered (single injection, flat tracing briefly)
- Panel 2 (right): Epinephrine (A) and Norepinephrine (B) given again → both still cause BP rise, but notice the responses are enhanced/exaggerated — peaks now reach ~180-200 mmHg
This pattern — where both epinephrine and norepinephrine show augmented pressor responses after drug X — indicates that drug X is a neuronal uptake blocker (Uptake-1 blocker).
1. Drug at Point X
Cocaine (or alternatively imipramine/desipramine — a Uptake-1/NET blocker)
The classic answer in pharmacology experiments is Cocaine, which blocks the norepinephrine transporter (NET/Uptake-1), preventing reuptake of catecholamines → potentiates and prolongs the pressor effects of both epinephrine and norepinephrine.
2. Type of Drug Interaction
Pharmacokinetic potentiation via inhibition of neuronal reuptake (Uptake-1 blockade)
| Feature | Explanation |
|---|---|
| Mechanism | Cocaine blocks NET (norepinephrine transporter) on sympathetic nerve terminals |
| Effect | More catecholamine remains in synapse → enhanced receptor activation |
| Result | Pressor responses to both Epi and NE are augmented |
| Interaction type | Pharmacokinetic (disposition/reuptake) → functional potentiation |
This is the cocaine-catecholamine potentiation experiment, a classic demonstration of Uptake-1 blockade in pharmacology.
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