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

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.

• ↓ Heart rate
• ↓ Cardiac output
• ↓ Peripheral vascular resistance

Unlike:

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

Clonidine acts centrally.

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

Common:

• Sedation
• Dry mouth
• Bradycardia
• Fatigue
• Constipation

Serious:

• Rebound hypertension (if abruptly stopped)

Abrupt discontinuation leads to:

• Sudden sympathetic surge
• Severe hypertension
• Tachycardia

Mechanism:

• Upregulated adrenergic receptors during therapy
• Sudden removal → exaggerated sympathetic response

Always taper slowly.

Compared to:

• ACE Inhibitors
• ARBs
• Calcium Channel Blockers
• Thiazide Diuretics

Clonidine:

• Not first-line
• No mortality benefit
• Reserved for refractory cases

Use caution in:

• Bradycardia
• Conduction disease
• Depression

Avoid abrupt withdrawal.

• 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

• Hypertension
• Beta-Blockers
• Calcium Channel Blockers
• Diuretics
• Cardiovascular Pharmacology