Passive Cigarette Smoking Impact on Blood Pressure Response to Epinephrine and Felypressin in 1K1C Hypertensive Rats Treated or not with Atenolol

Abstract Background: Cigarette smoking is usually associated with hypertension and may modify vasoconstrictor response. Objective: The present study aimed to analyze and compare the interaction of passive cigarette smoking and hypertension on epinephrine and felypressin blood pressure effects after intravascular injection. Method: 45-day male Wistar rats had the main left renal artery partially constricted and the right kidney removed (1K1C model). Rats were placed in the chamber for exposition to passive cigarette smoking (10 cigarettes) during 10 min (6 days a week). Hypertensive rats received atenolol (90 mg/kg/day) by gavage for two weeks. Hypotensive and hypertensive response, response duration and heart rate were recorded from direct blood pressure values. The significance level was 5%. Results: Passive cigarette smoking increased maximal hypertensive response to epinephrine in normotensive and 1K1C-atenolol treated rats and to felypressin only in 1K1C-atenolol treated rats; it also reduced epinephrine hypotensive response. Epinephrine increased heart rate in normotensive and hypertensive passive smokers or non-smoker rats. Comparing the two vasoconstrictors, epinephrine showed greater hypertensive response in normotensive smokers, 1K1C-atenolol treated smokers and non-smokers. However, in normotensive-nonsmoker rats, felypressin showed a greater and longer hypertensive effect. Conclusions: Our results suggest that passive cigarette smoking may reduce epinephrine vasodilation and increase hypertensive response when compared to felypressin. Therefore, felypressin may be safe for hypertensive patients to avoid tachycardia and atenolol interaction, but for normotensive and non-smoker patients, epinephrine may be safer than felypressin.

摘要：
背景：吸烟通常与高血压（hypertension）相关，并可调节血管收缩反应。
目的：本研究旨在分析并比较被动吸烟（passive cigarette smoking）与高血压对血管内注射后肾上腺素（epinephrine）和苯赖加压素（felypressin）血压效应的交互作用。
方法：选取45日龄雄性Wistar大鼠，对其左侧主肾动脉进行部分狭窄并摘除右侧肾脏，构建1肾1夹（1K1C）模型。将大鼠置于染毒舱中，每周6天、每次10分钟暴露于10支香烟产生的烟雾中。高血压大鼠经灌胃给予阿替洛尔（atenolol）90 mg/kg/天，持续2周。通过直接血压监测记录降压反应、升压反应、反应持续时间及心率，显著性水准设定为5%。
结果：被动吸烟可提升正常血压大鼠及1肾1夹+阿替洛尔处理大鼠对肾上腺素的最大升压反应，且仅在1肾1夹+阿替洛尔处理大鼠中提升对苯赖加压素的升压反应；同时可减弱肾上腺素的降压反应。在正常血压、高血压被动吸烟大鼠及非吸烟大鼠中，肾上腺素均可升高心率。对比两种血管收缩剂，肾上腺素在正常血压吸烟大鼠、1肾1夹+阿替洛尔处理吸烟大鼠及非吸烟大鼠中展现出更强的升压反应。但在正常血压非吸烟大鼠中，苯赖加压素的升压效应更强且持续更久。
结论：本研究结果提示，相较于苯赖加压素，被动吸烟可减弱肾上腺素的血管舒张作用并增强升压反应。因此，苯赖加压素用于高血压患者时可避免心动过速及与阿替洛尔的相互作用，安全性更佳；但对于正常血压非吸烟患者，肾上腺素相较苯赖加压素更为安全。