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# Vasopressors and inotropes by receptor and mechanism

- Concept

Vasopressors tighten blood vessels to raise blood pressure; inotropes make the heart squeeze harder. Each works on different receptors.

Updated Nov 13, 2026

## Key points

- Alpha-1 constricts vessels; beta-1 raises contractility and heart rate; beta-2 dilates vessels and bronchi and raises lactate; V1 constricts vessels without adrenergic receptors.
- Noradrenaline (mainly alpha-1 with some beta-1) is the first-line vasopressor in septic shock.
- Vasopressin is a non-catecholamine added to spare noradrenaline; it works in acidosis, where adrenergic receptors respond poorly.
- Dobutamine (mainly beta-1) and milrinone (phosphodiesterase-3 inhibitor) are inodilators: they raise output but can lower blood pressure.
- Phenylephrine is a pure alpha-1 agonist and can cause reflex bradycardia; adrenaline raises lactate through beta-2 effects.

On this page

- The basics Key points
- What it is
- Key points
- Components
- How it works
- Receptor profile and main effects
- In practice
- Next step
- Memory aid
- Elsewhere in DurgiPedia

- Study Test yourself

- Connections Connections

## What it is

Vasoactive drugs support the circulation in shock while the cause is treated. Vasopressors raise blood pressure mainly by constricting arterioles, increasing systemic vascular resistance; inotropes increase the force of cardiac contraction and so the cardiac output. Most act on adrenergic receptors. Alpha-1 receptors on vascular smooth muscle cause vasoconstriction; beta-1 receptors on the heart increase contractility and heart rate; beta-2 receptors relax vascular and bronchial smooth muscle and drive glycogenolysis and lactate production; dopamine receptors dilate renal and splanchnic vessels. Other agents bypass adrenergic receptors: vasopressin acts on V1 receptors on vessels, phosphodiesterase-3 inhibitors raise cyclic AMP in heart muscle and vessels, calcium sensitisers increase the response of troponin to calcium, and angiotensin II acts on AT1 receptors. Choosing an agent means matching its receptor profile to the patient's problem: low vascular tone, low cardiac output, or both. In septic shock noradrenaline is the usual first choice, vasopressin is often added, and adrenaline or an inotrope is considered when the heart is failing. These drugs are given through a dedicated line with continuous arterial monitoring, are titrated to effect and are weaned as soon as the patient allows; on DurgiPedia they are taught by mechanism only, without doses.

## Key points

- Vasopressors treat low vascular tone (distributive shock); inotropes treat low cardiac output (cardiogenic shock); some drugs do both.
- Catecholamines (noradrenaline, adrenaline, dopamine, dobutamine) act on adrenergic receptors and lose effect in severe acidosis and with receptor down-regulation.
- Non-adrenergic options (vasopressin, angiotensin II, phosphodiesterase-3 inhibitors, calcium sensitisers) help when catecholamines fail or cause arrhythmias.
- All vasopressors can cause tissue ischaemia of the gut, fingers and skin, and arrhythmias; the lowest effective dose for the shortest time is the principle.
- Extravasation from a peripheral vein can cause skin necrosis; a central line is preferred for prolonged use, and a large proximal peripheral vein can bridge for a short time.

## Components

- Noradrenaline: strong alpha-1, moderate beta-1 — raises vascular resistance and pressure with little rise in heart rate.
- Adrenaline: beta-1, beta-2 and alpha-1 — raises output and pressure; causes tachycardia, arrhythmias, high glucose and lactate.
- Vasopressin: V1 receptors on vascular smooth muscle — vasoconstriction independent of adrenergic receptors; V2 receptors in the kidney retain water.
- Phenylephrine: pure alpha-1 — raises resistance; may reduce output and slow the heart reflexly.
- Dopamine: dopamine, beta-1 and alpha-1 receptors, with effects that shift across its range — more arrhythmias, so rarely first choice now.
- Dobutamine: mainly beta-1 with some beta-2 — inotrope with mild vasodilation.
- Milrinone: phosphodiesterase-3 inhibitor — inotrope and vasodilator acting beyond the beta receptor; cleared by the kidneys.
- Levosimendan: calcium sensitiser and opener of ATP-sensitive potassium channels — inotropy and vasodilation without raising oxygen use much.
- Isoprenaline: beta-1 and beta-2 — raises heart rate; used for bradycardia as a bridge to pacing.

## How it works

- Alpha-1 receptors are coupled to Gq: phospholipase C raises intracellular calcium and contracts vascular smooth muscle.
- Beta-1 and beta-2 receptors are coupled to Gs: cyclic AMP rises; in the heart it increases calcium entry and contraction, in vessels it relaxes muscle.
- Phosphodiesterase-3 inhibitors stop cyclic AMP breakdown, so they work even when beta receptors are blocked or down-regulated.
- V1 receptors are also Gq-coupled; vasopressin levels fall in prolonged septic shock, which is one reason replacing it helps.
- Corticosteroids restore vascular responsiveness to catecholamines and are added in septic shock that needs escalating vasopressors.

## Receptor profile and main effects

| Drug | Main receptors | Main effect | Typical use |
| --- | --- | --- | --- |
| Noradrenaline | Alpha-1 more than beta-1 | Vasoconstriction | Septic and most distributive shock |
| Adrenaline | Beta-1, beta-2, alpha-1 | Inotropy and vasoconstriction | Anaphylaxis, cardiac arrest, refractory shock |
| Vasopressin | V1 (non-adrenergic) | Vasoconstriction | Added to noradrenaline in septic shock |
| Phenylephrine | Alpha-1 only | Vasoconstriction, reflex slow heart | Short-term hypotension, e.g. after anaesthesia |
| Dobutamine | Beta-1 more than beta-2 | Inotropy, mild vasodilation | Low-output cardiogenic shock |
| Milrinone | Phosphodiesterase-3 inhibition | Inotropy and vasodilation | Low output, right heart failure, beta-blockade |

## In practice

- Septic shock: noradrenaline first, add vasopressin when needs keep rising, consider adrenaline or an inotrope if the heart is failing.
- Cardiogenic shock: an inotrope for low output, often with noradrenaline to hold pressure; urgent reperfusion if an infarction is the cause.
- Anaphylaxis: adrenaline treats both vasodilation and bronchospasm and stabilises mast cells.
- Beta-blocker overdose or a patient on beta-blockers: phosphodiesterase-3 inhibitors and glucagon act beyond the beta receptor.
- Watch for cold, mottled fingers, rising lactate from gut ischaemia, new arrhythmias and high glucose as side effects.

## Next step

- Run vasoactive drugs through a dedicated lumen with an arterial line; label each line and avoid flushes through it.
- Reassess the cause and fluid status every time vasopressor needs rise; call the senior intensivist when a second agent is considered.
- Check the peripheral cannula site often if a central line is not yet in place; stop and treat extravasation at once.
- Follow lactate, glucose, rhythm and limb perfusion as markers of benefit and harm.
- Wean one agent at a time as shock resolves, usually stopping the drug added last before noradrenaline.

## Memory aid

Alpha tightens, Beta-1 beats, Beta-2 breathes and bleeds lactate, V1 squeezes when the rest give up.

## Test yourself

Think of the answer, then tap the question to see it.

## Why is noradrenaline the usual first vasopressor in septic shock?

Its strong alpha-1 effect restores vascular tone, and its modest beta-1 effect supports the heart with less tachycardia and fewer arrhythmias than dopamine.

## How does vasopressin raise blood pressure?

It acts on V1 receptors on vascular smooth muscle, a non-adrenergic pathway, so it still works in acidosis and spares catecholamine use.

## Why can milrinone work in a patient taking beta-blockers?

It inhibits phosphodiesterase-3 and raises cyclic AMP downstream of the beta receptor, so it does not need the receptor to be free.

## Why may adrenaline raise lactate without worse perfusion?

Its beta-2 effect stimulates glycogenolysis and glycolysis in muscle, producing lactate even when tissues are adequately perfused.

[Add to my cards (4)](https://durgical.app/estudiar/?add=/en/anaesthesia/vasopressors-and-inotropes-by-receptor-and-mechanism/)

## Elsewhere in DurgiPedia

- [Preload, afterload and contractility](https://durgical.com/en/physiology/preload-afterload-and-contractility/)
- [Flow, pressure and resistance: Poiseuille and turbulent flow](https://durgical.com/en/physiology/flow-pressure-and-resistance-poiseuille-and-turbulent-flow/)
- [Shock physiology](https://durgical.com/en/physiology/shock-physiology/)
- [Central venous catheter care](https://durgical.com/en/nursing/central-venous-catheter-care/)

## Connections

## Related 6

- [Shock: a bedside approach by type](https://durgical.com/en/anaesthesia/shock-a-bedside-approach-by-type/)
- [Haemodynamic monitoring: arterial line, CVP, cardiac output and lactate](https://durgical.com/en/anaesthesia/haemodynamic-monitoring-arterial-line-cvp-cardiac-output-and-lactate/)
- [Central lines in the ICU: choice, checks and removal](https://durgical.com/en/anaesthesia/central-lines-in-the-icu-choice-checks-and-removal/)
- [Intraoperative hypotension](https://durgical.com/en/anaesthesia/intraoperative-hypotension/)
- [Advanced life support in hospital](https://durgical.com/en/anaesthesia/advanced-life-support-in-hospital/)
- [Anaphylaxis under anaesthesia](https://durgical.com/en/anaesthesia/anaphylaxis-under-anaesthesia/)

## Related conditions 5

- [Sepsis and septic shock](https://durgical.com/en/conditions/sepsis-and-septic-shock/)
- [Cardiogenic shock](https://durgical.com/en/conditions/cardiogenic-shock/)
- [Anaphylaxis](https://durgical.com/en/conditions/anaphylaxis/)
- [Heart failure](https://durgical.com/en/conditions/heart-failure/)
- [Neurogenic shock](https://durgical.com/en/conditions/neurogenic-shock/)

## In Pharmacology 12

- [Vasopressors and inotropes](https://durgical.com/en/pharmacology/classes/vasopressors-and-inotropes/)
- [Norepinephrine](https://durgical.com/en/pharmacology/norepinephrine/)
- [Epinephrine](https://durgical.com/en/pharmacology/epinephrine/)
- [Vasopressin](https://durgical.com/en/pharmacology/vasopressin/)
- [Phenylephrine](https://durgical.com/en/pharmacology/phenylephrine/)
- [Dopamine](https://durgical.com/en/pharmacology/dopamine/)
- [Dobutamine](https://durgical.com/en/pharmacology/dobutamine/)
- [Milrinone](https://durgical.com/en/pharmacology/milrinone/)
- [Levosimendan](https://durgical.com/en/pharmacology/levosimendan/)
- [Isoprenaline](https://durgical.com/en/pharmacology/isoprenaline/)
- [Ephedrine](https://durgical.com/en/pharmacology/ephedrine/)
- [Hydrocortisone](https://durgical.com/en/pharmacology/hydrocortisone/)

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Educational content; it does not replace supervised training, your institution's protocols or the anaesthetist's or intensivist's decision. It contains no doses and no ventilator or infusion settings.

Sources: [Inotropes and Vasopressors](https://www.ncbi.nlm.nih.gov/books/NBK482411/) (StatPearls (NCBI Bookshelf), 2024).

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Representative model, for educational purposes only.

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Source: https://durgical.com/en/anaesthesia/vasopressors-and-inotropes-by-receptor-and-mechanism/
License: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Cite as: DurgiPedia (durgical.com), https://durgical.com/en/anaesthesia/vasopressors-and-inotropes-by-receptor-and-mechanism/