{'fraction_non_alphanumeric': 0.010416666666666666, 'fraction_numerical': 0.005208333333333333, 'mean_word_length': 6.014598540145985, 'pattern_counts': {'":': 0, '<': 0, '<?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}}
Angiotensin type 1A receptor expression in C1 neurons of the rostral ventrolateral medulla contributes to the development of angiotensin‐dependent hypertension

What is the central question of this study? This study addresses the mechanism by which deletion of angiotensin II type 1A receptors from catecholaminergic neurons reduces angiotensin‐dependent hypertension, as well as the identity of the cells involved. What is the main finding and its importance? Deletion of angiotensin II type 1A receptors from catecholaminergic neurons results in reduced sympathetic nerve activation and fluid and electrolyte retention during angiotensin infusion. The C1 neurons of the rostral ventrolateral medulla are involved in the later phase of the hypertension. We demonstrate that at least two different populations of catecholaminergic neurons are involved in the sympathetic nerve activation required for the full development of angiotensin‐dependent hypertension.