Everyday life is full of events that can cause stress. Exposure to chronic stress is linked to a number of diseases such as depression, heart disease, and hypertension. Stress causes an increase in circulating glucocorticoid and sympathetic nervous system output, commonly referred to as the fight-flight response. However, it is not clear whether the actual stress stimulus is required or if repeated activation of the fight-flight responses in the absence of a physical/psychological stressor is sufficient to cause impaired health outcomes. In this study we sought to develop a method to gain control over neurons that control fight-flight responses. Rats were put under an anesthetic and a virus was injected into the Rostral-Ventrolateral Medulla (RVLM), a brainstem nuclei that controls the stress response. The virus infects neurons with a vector that causes the expression of Designer Receptor Exclusively Activated by Designer Drugs (DREADDs) giving us control over the activation of these neurons. After three weeks, experimental animals were anesthetized and electrocardiogram electrodes attached for monitoring heart rate. Animals injected with the designer drug, clozapine-n-oxide (CNO) that activates neurons expressing DREADDs showed a spike in heart rate forty minutes after injection and a general increase thereafter. In contrast, control animals injected with saline showed a slow gradual decrease in heart rate. This study demonstrated we could gain control over the fight-flight response of an animal without physically exposing it to an actual stressor.