{'fraction_non_alphanumeric': 0.02525497814473045, 'fraction_numerical': 0.007770762506070908, 'mean_word_length': 6.152777777777778, '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}}
Brainstem adrenomedullin facilitates intermittent hypoxia‐induced hypertension: A sympathetic story of a selfish brain

There is considerable interest in the mechanism(s) of chronic intermittent hypoxia (CIH)-induced hypertension in the continued search for a fundamental understanding of the elaboration of cardiovascular morbidity in persons with obstructive sleep apnoea. In the September issue of Experimental Physiology, Zoccal et al. (2019) explore whether centrally acting adrenomedullin is implicated in the persistent sympathetic nervous hyperactivity that is characteristic of animal models of CIH and human sleep apnoea and that is considered causal to the development of high blood pressure. Adrenomedullin is a multifunctional vasoactive peptide member of the calcitonin gene-related peptide family of hormones (Schönauer, Els-Heindl, & Beck-Sickinger, 2017). It is expressed in various tissues, including the adrenal glands, kidneys and heart, and can enter the brain from the circulation via the area postrema. In addition, adrenomedullin is synthesized by neurons in specific brain areas, including those crucially involved in autonomic control of the cardiovascular system (Hwang & Tang, 1999). Of interest, hypoxia increases the expression of central adrenomedullin, purportedly as part of a generic protective response, providing rationale for a potential role of the sympatho-excitatory peptide in the manifestation of CIH-induced hypertension. Zoccal et al. (2019) used the established working heart–brainstem preparation to record phrenic nerve and thoracic sympathetic nerve activities in shamand CIH-exposed rats to determine respiratory and autonomic responses to adrenomedullin receptor agonism and antagonism via microinjections into the rostral ventrolateral medulla (RVLM), with and without concomitant repeated peripheral arterial chemoreceptor stimulation using potassium cyanide. In CIH-exposed rats, baseline sympathetic activity and sympatho-excitatory responses to peripheral chemoreceptor activation were increased compared