Clonidine

Clonidine is a centrally acting alpha-2 adrenergic agonist.

It lowers blood pressure by reducing sympathetic outflow from the central nervous system.

Used in:

Resistant Hypertension
Hypertensive urgency
ADHD (non-cardiovascular indication)
Opioid withdrawal

Mechanism of Action

Clonidine stimulates central alpha-2 receptors in the brainstem.

Normal physiology:

Sympathetic tone increases:
- Heart rate
- Contractility
- Peripheral vascular resistance

Alpha-2 activation causes:

↓ Sympathetic outflow
↓ Norepinephrine release
↓ Heart rate
↓ Cardiac output
↓ Systemic vascular resistance

Net effect:

↓ MAP (Mean Arterial Pressure)

Primary action = central sympatholysis.

Hemodynamic Effects

↓ Heart rate
↓ Cardiac output
↓ Peripheral vascular resistance

Unlike:

Beta-Blockers (peripheral blockade)
Calcium Channel Blockers (vascular smooth muscle)

Clonidine acts centrally.

Clinical Use

Resistant Hypertension:

Add-on agent when standard therapy insufficient

Hypertensive Urgency:

Oral option for gradual BP reduction

Opioid Withdrawal:

Reduces autonomic hyperactivity

ADHD:

Central modulation

Adverse Effects

Common:

Sedation
Dry mouth
Bradycardia
Fatigue
Constipation

Serious:

Rebound hypertension (if abruptly stopped)

Rebound Hypertension

Abrupt discontinuation leads to:

Sudden sympathetic surge
Severe hypertension
Tachycardia

Mechanism:

Upregulated adrenergic receptors during therapy
Sudden removal → exaggerated sympathetic response

Always taper slowly.

Clonidine vs Other Agents

Compared to:

Clonidine:

Not first-line
No mortality benefit
Reserved for refractory cases

Contraindications & Caution

Use caution in:

Bradycardia
Conduction disease
Depression

Avoid abrupt withdrawal.

Clinical Pearls

Central alpha-2 agonist
Reduces sympathetic tone
Causes sedation and dry mouth
Risk of rebound hypertension
Not first-line for chronic HTN
Useful in hypertensive urgency