Increased vasopressin transmission from the paraventricular nucleus to the rostral medulla augments cardiorespiratory outflow in chronic intermittent hypoxia‐conditioned rats

摘要: A co-morbidity of sleep apnoea is hypertension associated with elevated sympathetic nerve activity (SNA) which may result from conditioning to chronic intermittent hypoxia (CIH). Our hypothesis that SNA depends on input the rostral ventrolateral medulla (RVLM) neurons in paraventricular nucleus (PVN) release arginine vasopressin (AVP) and specifically, increased evoked by CIH this excitatory input. In two sets neuroanatomical experiments, we determined if AVP project PVN RVLM (V1A) receptor expression increases after (8 h per day for 10 days). first set, cholera toxin β subunit (CT-β) was microinjected into retrogradely label neurons. Immunohistochemical staining demonstrated 14.6% CT-β-labelled were double-labelled AVP. second sections immunolabelled V1A receptors, receptor-expressing cell count significantly greater (P < 0.01) neighbouring ventral respiratory column (rVRC) CIH- than room air (RA)-conditioned rats. a series physiological blocking receptors would normalize blood pressure CIH-conditioned animals attenuate its response disinhibition PVN. Blood (BP), heart rate (HR), diaphragm (DEMG) genioglossus muscle (GGEMG) recorded anaesthetized, ventilated vagotomized The disinhibited microinjecting GABAA antagonist, bicuculline (BIC, 0.1 nmol), before within rVRC SR49059 (0.2 nmol). RA-conditioned rats, BP, HR, minute DEMG GGEMG these attenuated receptors. dose blocker (0.4 nmol) required blunt responses 0.05). Further, normalized baseline BP. summary, released subset modulates cardiorespiratory output via rVRC, up-regulation RVLM.