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Korean Circ J. 1999 Apr;29(4):403-407. Korean. Original Article. https://doi.org/10.4070/kcj.1999.29.4.403
Park KS , Kong ID , Park KC , Lee JW .
Abstract

BACKGROUND: One of the most common side effects of antidepressant medication is orthostatic hypotension, which can be caused by impaired vasoconstriction. This study was designed to compare the inhibitory effects of antidepressants, including selective serotonin reuptake inhibitors (SSRIs), on the contractile responses to alpha1-adrenergic receptor activation and depolarization in isolated rat aorta. METHODS: Vascular rings were suspended for the measurement of isometric tension in a water-jacketed bath filled with Tyrode solution. After pretreatment with antidepressant for 20 min, vasoconstriction induced by norepinephrine (NE) or 35 mM K+ was measured and compared to the control response. RESULTS: Whereas trazodone and tricyclic antidepressants (TCAs) selectively inhibited NE-induced vasoconstriction, SSRIs inhibited depolarization-induced vasoconstriction more potently. The IC50 value of fluoxetine on depolarization- induced vasoconstriction was 3.29 microM, which is consistent with the previous results on L-type Ca2+ currents of cardiac myocyte. Moclobemide, a monoamine oxidase inhibitor, had no effect on vasoconstriction induced by either alpha- adrenergic receptor activation, or depolarization. CONCLUSION: These results suggest that SSRIs, different from TCAs and trazodone, have potent inhibitory actions to depolarization-induced contraction that may be due to blocking Ca2+ entry through L-type Ca2+ channel.

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