{'fraction_non_alphanumeric': 0.059516023544800525, 'fraction_numerical': 0.04447351209941138, 'mean_word_length': 4.7518796992481205, 'pattern_counts': {'":': 0, '<': 5, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Stress induced activation of brain regions in genetically hypertensive mice

The high blood pressure (BPH) strain of "Schlager" mice have greater arousal associated rises in blood pressure compared with normotensive mice (BPN). To elucidate whether this is due to a neurogenic mechanism, we examined brain regions activated by acute aversive stress that may contribute to the hypertension. BPN and BPH mice were implanted with telemetry devices to measure cardiovascular variables at rest and throughout a 1 hr cage swap stress. Neuronal activation was detected using c‐Fos‐immunohistochemistry. Greater resting mean arterial pressure (MAP) was recorded in BPH mice (102±2 mmHg; n = 5) than in BPN mice (86±1 mmHg; n = 7). Heart rate (HR) levels were also elevated in BPH mice (438±11 bpm) compared with BPN mice (338±5 bpm). Cage swap increased MAP more in BPH compared to BPN mice (+41±2 vs +31±1 mmHg, P < 0.001), as did activity (+6.3±0.5 vs +2.6±0.2 units, P < 0.001). By contrast, HR increased less in BPH mice (+275±13 vs +356±15 bpm, P < 0.001). Exposure to acute stress induced 33% greater neuronal activation in the paraventricular nucleus (P < 0.05) and 27% greater in the dorsomedial hypothalamus (P < 0.001) in BPH (n = 3) compared to BPN mice (n = 3). A relatively "natural" arousal response induces a markedly greater activation of brain regions important for regulating cardiovascular autonomic function. The greater pressor response to stress suggests a central mechanism may be contributing to the hypertension.