It is known that some drugs can cause depression. In particular, there is evidence that barbiturates, vigabatrine, topiramate, şunarizine, corticosteroids, meşoquine, efavirenz, and interferon alpha have been shown to cause depression (1). Angiotensin II is a strong vasopressor with various physiological effects especially regulating blood pressure. It regulates water retention and aldosterone secretion. Angiotensin II has two known receptors, AT1 and AT2. Valsartan is a non-selective angiotensin AT selective blocker, which prevents angiotensin binding to AT2 receptors and controls hypertension in this way (2). It has been shown that angiotensin converting enzyme polymorphism is related to relapse in major depression patients after partial sleep deprivation and this was related to its effect on the dopaminergic system (3). This finding shows that drugs targeting the angiotensin system may effect depression. Here we present a case with recurrent depression who was in remission and relapsed after she was given an antihypertensive medication containing valsartan and hydrochlorothiazide. She was a 56 year old single woman, living alone. She had a depressive episode in 1983 for the first time and had other episodes in 1997, 2001, and the last one in 2003. After having used venlafaxine and paroxetine, she was given citalopram in 2003 at 40 mg/day, which she has been using until now. She did not have any depressive attacks after 2003. She was given an antihypertensive containing valsartan and hydrochlorothiazide 3 months before she presented to our clinic. After taking the medication she had reluctance, despondency, intense feelings of guilt with statements like "she will not be even accepted to hell." There were no stressors that the patient or her relatives defined. The patient was admitted to our clinic after her symptoms increased the month prior to her admission. Since there were published articles on depression triggered by valsartan and similar antihypertensives and since the patient's symptoms started after taking the medication, we continued on her drug regimen with citalopram 40 mg/day and changed her antihypertensive medication to a calcium channel blocker, amlodipine. After 2 weeks her symptoms started to decrease. We concluded that her depression was triggered by valsartan. This case is important for showing that medications affecting the angiotensin system can trigger depression and there is a need to study the role of the angiotensin system in the etiology of depression.
References:
1. Celano CM, Freudenreich O, Fernandez-Robles C, Stern TA, Caro MA, Huffman JC. Depressogenic effects of medications: a review.Dialogues Clin Neurosci. 2011;13(1):109-25.
2. Black HR, Bailey J, Zappe D, Samuel R.Valsartan: more than a decade of experience. Drugs. 2009;69(17):2393-414. Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S198