Certain treatments—rather than depression itself—may contribute to hypertension

The long-held notion that depression and anxiety can elevate your blood pressure certainly seems plausible. After all, a mood or anxiety disorder—and the toll it takes on your life—leads to chronic stress, which contributes to hypertension. Plus, depression is a known risk factor for heart disease, and it was often assumed that high blood pressure partly explained the link.

While recent evidence affirms the link between anxiety and elevated blood pressure, it does not do the same for depression and hypertension. In fact, investigators are finding that people with depression are more likely to have low blood pressure than those without depression.

When depressed individuals do have hypertension, it could be caused by certain antidepressant medications—namely tricyclics or serotonin and norepinephrine reuptake inhibitors (SNRIs).

The Antidepressant-Hypertension Link

Several studies in the past decade have found that, contrary to the prevailing consensus, depression is actually linked with low blood pressure. One of the most recent is a 2009 article published in Hypertension in which researchers in the Netherlands looked at depression and blood pressure in 2,618 adults ages 18 to 65.

Scientists divided the participants into three groups: those who had no history of anxiety or depression; those who had depression or anxiety but did not take antidepressants; and those who took antidepressants for depression or anxiety. The majority of the participants on medication (442) took a selective serotonin reuptake inhibitor (SSRI), the most popular class of antidepressants that includes fluoxetine (Prozac) and escitalopram (Lexapro). One hundred thirty-five took a drug from the related SNRI class, such as duloxetine (Cymbalta) or venlafaxine (Effexor), and 67 took a tricyclic medication, an older class of antidepressants that includes nortriptyline (Pamelor) and desipramine (Norpramin).

The researchers also measured the participants' blood pressure levels and adjusted the numbers for those who were taking blood pressure medication. Sixty-four percent of the participants had no hypertension, 16 percent had isolated systolic hypertension (only the top number was elevated), 3 percent had isolated diastolic hypertension (only the bottom number was elevated), 13 percent had hypertension stage 1 (at least 140/90 mm Hg), and 5% had hypertension stage 2 (at least 160/100 mm Hg).

Surprisingly, a higher systolic blood pressure reading and isolated systolic hypertension were more common in participants without depression than in those with the disorder. People taking SSRIs did not seem to have an increased risk of high blood pressure, and those taking SNRIs had a slightly increased risk of stage 1 hypertension. But people taking tricyclic antidepressants had double the risk of hypertension stage 1 and almost triple the risk of hypertension stage 2.

A 2010 study of about 4,000 U.S. adults ages 45 to 84 found comparable results. After a year and a half, people with depression had similar blood pressure levels and were no more likely to develop hypertension than those without depression. But among the participants taking an antidepressant, those who used a tricyclic drug were 20 percent more likely to develop hypertension than those who took another type of medication. This study did not separate out SNRI users from the nontricyclic group.

What To Do

It is too soon to say that tricyclic and SNRI antidepressants definitively cause high blood pressure. However, if you have hypertension or are at risk for it, you and your doctor should weigh the risks and benefits of these drugs before starting on one. Under these circumstances, an SSRI, which has no effect on blood pressure, may be a more appropriate antidepressant choice.

But if you're already taking a tricyclic or SNRI, there is no need to switch to an SSRI—unless problems with blood pressure control begin to arise. So make sure that your doctor monitors your blood pressure at each visit.

Publication Review By: Karen L. Swartz, M.D.

Published: 20 Aug 2013

Last Modified: 20 Aug 2013