Research suggests that chronic stress and subsequent activation of the sympathetic nervous system contribute to the development of hypertension. Recent work suggests that pituitary adenylate cyclase‐activating polypeptide (PACAP)‐dependent mechanisms sustain sympathoadrenal responses to prolonged but not acute stress. Group‐housed rats were placed in a sound chamber 25 cm from speakers randomly emitting four pure tones (5, 11, 15, and 19 kHz) for 30 min. After daily sound stress for 4 weeks rats were lightly anesthetized (isoflurane: 4% induction; 1.75% maintenance) and blood pressure was measured by tail‐cuff plethysmography. Stressed rats did not exhibit changes in diastolic blood pressure but showed a significant increase in systolic blood pressure compared to age‐matched controls: 118.3 ± 1.6 and 96.9 ± 1.7 mmHg, respectively (n=8; p<0.05) suggesting increased sympathetic drive originating in central autonomic and/or pre‐autonomic nuclei. Following blood pressure measurement, brains were removed and tissue from the hypothalamic paraventricular nucleus (PVN) was subjected to qPCR. In pilot experiments we observed elevated gene expression for PACAP (normalized to ribosomal protein L30) in stressed animals (9.10 ± 4.73) versus controls (1.12 ± 0.26; n=8; p=0.1). A similar elevation was observed for the PACAP receptor PAC1R: 5.27 ± 2.47 and 1.12 ± 0.21, respectively (n=8, p=0.1).