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Effects of β‐adrenoceptor activation on haemodynamics during hypoxic stress in rats
Author(s) -
Ji Qiaorong,
Zhang Yu,
Zhang Huan,
Liu Jie,
Cao Chengzhu,
Yuan Zhouyang,
Ma Qianqian,
Zhang Wei
Publication year - 2020
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/ep088669
Subject(s) - atenolol , hemodynamics , propranolol , heart rate , blood pressure , hypoxia (environmental) , anesthesia , medicine , catecholamine , cardiac output , vascular resistance , pulmonary artery , mean arterial pressure , endocrinology , chemistry , organic chemistry , oxygen
New FindingsWhat is the central question of this study? The acute hypoxic compensatory reaction is based on haemodynamic changes, and β‐adrenoceptors are involved in haemodynamic regulation. What is the role of β‐adrenoceptors in haemodynamics during hypoxic exposure?What is the main finding and its importance? Activation of β 2 ‐adrenoceptors attenuates the increase in pulmonary artery pressure during hypoxic exposure. This compensatory reaction activated by β 2 ‐adrenoceptors during hypoxic stress is very important to maintain the activities of normal life.Abstract The acute hypoxic compensatory reaction is accompanied by haemodynamic changes. We monitored the haemodynamic changes in rats undergoing acute hypoxic stress and applied antagonists of β‐adrenoceptor (β‐ARs) subtypes to reveal the regulatory role of β‐ARs on haemodynamics. Sprague–Dawley rats were randomly divided into control, atenolol (β 1 ‐AR antagonist), ICI 118,551 (β 2 ‐AR antagonist) and propranolol (non‐selective β‐AR antagonist) groups. Rats were continuously recorded for changes in haemodynamic indexes for 10 min after administration. Then, a hypoxic ventilation experiment [15% O 2 , 2200 m a.sl., 582 mmHg (0.765 Pa), P O 287.3 mmHg; Xining, China] was conducted, and the indexes were monitored for 5 min after induction of hypoxia. Plasma catecholamine concentrations were also measured. We found that, during normoxia, the mean arterial pressure, heart rate, ascending aortic blood flow and pulmonary artery pressure were reduced in the propranolol and atenolol groups. Catecholamine concentrations were increased significantly in the atenolol group compared with the control group. During hypoxia, mean arterial pressure and total peripheral resistance were decreased in the control, propranolol and ICI 118,551 groups. Pulmonary arterial pressure and pulmonary vascular resistance were increased in the propranolol and ICI 118,551 groups. During hypoxia, catecholamine concentrations were increased significantly in the control group, but decreased in β‐AR antagonist groups. In conclusion, the β 2 ‐AR is involved in regulation of pulmonary haemodynamics in the acute hypoxic compensatory reaction, and the activation of β 2 ‐ARs attenuates the increase in pulmonary arterial pressure during hypoxic stress. This compensatory reaction activated by β 2 ‐ARs during hypoxic stress is very important to maintain activities of normal life.