Serotonin-norepinephrine Reuptake Inhibitors
Venlafaxine is a serotonin-norepinephrine reuptake inhibitor (SNRI) used in the treatment of depression and anxiety disorders. The likely mechanism of venlafaxine-induced hypertension is the increase in levels of norepinephrine and the subsequent potentiation of noradrenergic neurotransmission. The extended-release formulation of venlafaxine increases blood pressure in approximately 3% of patients when normal doses (75-150mg) are used. The majority of these blood pressure elevations, however, were considered minor. Doses ≥300 mg of extended-release venlafaxine demonstrated clinically significant elevations in 13% of patients, with the majority of blood pressure increases between 10 and 15 mmHg. However, it is important to note that dosing 300 mg or more is not common, and therisk of venlafaxine-induced hypertension will usually not warrant the discontinuation of this drug.
The clinical significance of sibutramineinduced hypertension is not well defined. Sibutramine is an SNRI and is chemically similar to amphetamine. Sibutramine’s likely mechanism of blood pressure elevation in both normotensive and hypertensive patients is the elevated amount of norepinephrine present in the body. A clinical trial evaluating the adverse reactions induced by sibutramine demonstrated a mean elevation of systolic and diastolic blood pressures of 2 mmHg in previously normotensive patients receiving 10 to 15 mg sibutramine daily. Interestingly, an elevation of 7 mmHg was demonstrated in hypertensive patients receiving similar doses. Other trials have demonstrated similar findings.[43,44] Patients with established hypertension receiving sibutramine experienced significantly higher elevations in blood pressure than patients who had normal blood pressure before medication initiation. Sibutramine treatment should probably be limited to patients who do not have cardiovascular disease, including hypertension, functional abnormalities, and coronary artery disease.