Drug group | Mechanism of hypotension and comments |
Diuretics - Loop diuretics (eg, furosemide, torsemide) or thiazides
| Extracellular fluid volume depletion. |
Adrenergic antagonists |
- Alpha-1-adrenergic blockers (eg, alfuzosin, tamsulosin, terazosin)
| Alpha-1-adrenergic blockers produce vasodilation via direct effect in vascular smooth muscle. |
- Beta-adrenergic blockers (eg, propranolol)
| Beta-adrenergic blockers reduce cardiac output and renin release. May also reduce vascular peripheral resistance. |
Alpha-2-adrenergic agonists (eg, tizanidine, clonidine) | Vasodilation via central inhibition of sympathetic efferent activity. |
Nitric oxide-mediated vasodilators - Nitroglycerin, hydralazine
- Phosphodiesterase-5-inhibitors (eg, sildenafil)
| Vasodilation via direct effect in vascular smooth muscle. |
Renin-angiotensin system (RAS) inhibitors (eg, lisinopril, valsartan) | Vasodilation via RAS inhibition. |
Calcium-channel blockers (eg, verapamil, diltiazem) | Reduction of cardiac output, vasodilation via direct effect in vascular smooth muscle. |
Dopamine antagonists - Phenothiazines (eg, chlorpromazine)
- Atypical antipsychotics (eg, olanzapine, risperidone, quetiapine)
| Vasodilation via central inhibition of sympathetic efferent activity. |
Antidepressants (eg, trazodone, amitriptyline) | Vasodilation via central and peripheral inhibition of sympathetic efferent activity through stimulation of adrenergic receptors. |
Selective serotonin receptor reuptake inhibitors (eg, paroxetine) | Unknown mechanism, possibly via central and peripheral inhibition of sympathetic efferent activity through stimulation of alpha-2-adrenergic receptors. |
Sodium-glucose co-transporter 2 inhibitors (eg, empagliflozin, canagliflozin) | Volume depletion via osmotic diuresis. |